To see the other types of publications on this topic, follow the link: Peptide natriuretico atriale.
Journal articles on the topic 'Peptide natriuretico atriale'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Peptide natriuretico atriale.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Wigle, D. A., B. M. Bennett, D. B. Jennings, I. R. Sarda, T. G. Flynn, and S. C. Pang. "Biological effects of rat iso-atrial natriuretic peptide and brain natriuretic peptide are indistinguishable from each other." Canadian Journal of Physiology and Pharmacology 70, no. 11 (November 1, 1992): 1525–28. http://dx.doi.org/10.1139/y92-218.
Full textAbstract:
Rat brain natriuretic peptide (rBNP) and iso-atrial natriuretic peptide (iso-rANP) were discovered independently by two research laboratories. They are considered to be members of the B-type natriuretic peptides. Except for the Gln/Leu substitution at position 44, the amino acid sequence of iso-rANP is identical with that of the C-terminal 45 amino acids of rat pro-BNP and with the 5-kDa cardiac peptide from rat atria. To determine whether this amino acid substitution can modify the known biological effects of rBNP and iso-rANP, the present investigation examined the cardiovascular and renal responses, vasorelaxant effect, receptor binding characteristics, and cyclic GMP production by the two peptides in relation to that of rat atrial natriuretic peptide (rANP). Results indicate that rBNP and iso-rANP are indistinguishable from each other in terms of these known biological activities of atrial natriuretic peptide. We therefore conclude that rBNP and iso-rANP are identical peptides and that the amino acid substitution at position 44 represents a polymorphic form of the rat B-type natriuretic peptide.Key words: atrial natriuretic peptide, brain natriuretic peptide, cardiovascular response, vasorelaxation, cyclic GMP, receptor binding.
2
Cozza, Eduardo N., Mark F. Foecking, Maria del Carmen Vila, and Celso E. Gomez-Sanchez. "Adrenal receptors for natriuretic peptides and inhibition of aldosterone secretion in calf zona glomerulosa cells in culture." Acta Endocrinologica 129, no. 1 (July 1993): 59–64. http://dx.doi.org/10.1530/acta.0.1290059.
Full textAbstract:
Atrial and brain natriuretic peptides specifically bind to primary cultures of calf adrenal glomerulosa cells. Binding of both natriuretic peptides to the same receptor has been proved by: a Dixon plot showing competitive effects for the binding of 125I-labeled brain natriuretic peptide in the presence of increasing concentrations of unlabeled atrial natriuretic peptide; a Scatchard plot showing a lower dissociation constant (Kd) for atrial natriuretic peptide than for brain natriuretic peptide binding, but the maximum binding (Bmax) values were the same; autoradiography of sodium dodecyl sulfate polyacrylamide gels after cross-linking of 125I-labeled atrial natriuretic peptide and 125I-labeled brain natriuretic peptide, showing the same molecular weights for both peptide receptors—a single 66-kD band in whole cells and a main band at 125 kD in membranes. C-Type atrial natriuretic peptide only slightly displaced atrial natriuretic peptide binding. Angiotensin II- and potassium-mediated stimulation of aldosterone production were inhibited strongly and to the same degree by atrial and brain natriuretic peptide but only slightly by C-type atrial natriuretic peptide. Stimulation of aldosterone production mediated by adrenocorticotropin was only partially inhibited by atrial and brain natriuretic peptide, while baseline aldosterone was not affected. These results suggest that atrial and brain natriuretic peptide bind to the same receptors and provoke the same effects on aldosterone production. The weak effects found with C-type atrial natriuretic peptide suggest that the primary culture of calf adrenal glomerulosa cells contain the guanylate cyclase A receptor.
3
VILLA, Giorgio LA, Massimo MANNELLI, Chiara LAZZERI, Sabrina VECCHIARINO, Maria Laura DE FEO, Cristina TOSTI GUERRA, Renzo BANDINELLI, Marco FOSCHI, and Franco FRANCHI. "Different effects of atrial and C-type natriuretic peptide on the urinary excretion of endothelin-1 in man." Clinical Science 95, no. 5 (November 1, 1998): 595–602. http://dx.doi.org/10.1042/cs0950595.
Full textAbstract:
1.Following the observation that brain natriuretic peptide enhances the urinary excretion rate of endothelin-1, the relationship between natriuretic peptides and urinary endothelin-1 was further investigated. Six healthy volunteers received, on three different occasions, increasing doses of atrial or C-type natriuretic peptide (0, 2 and 4 ;pmol·min-1·kg-1 for 1 ;h each), or placebo. 2.Atrial natriuretic peptide caused significant increases in the urinary excretion of cGMP, sodium and endothelin-1, without affecting plasma endothelin-1, renal plasma flow, glomerular filtration rate and urine flow rate. C-type natriuretic peptide did not modify any of these parameters. During atrial natriuretic peptide infusion, urinary endothelin-1 directly correlated with plasma atrial natriuretic peptide, urinary cGMP and sodium excretion. 3.These results indicate that enhancement of the urinary excretion of endothelin-1 by natriuretic peptides is dose-dependent and somewhat related to their ability to bind to natriuretic peptide receptors A, activate guanylate cyclase and induce a natriuretic response.
4
Mendelsohn, F. A. O., A. M. Allen, S. Y. Chai, P. M. Sexton, and R. Figdor. "Overlapping distributions of receptors for atrial natriuretic peptide and angiotensin II visualized by in vitro autoradiography: morphological basis of physiological antagonism." Canadian Journal of Physiology and Pharmacology 65, no. 8 (August 1, 1987): 1517–21. http://dx.doi.org/10.1139/y87-239.
Full textAbstract:
Atrial natriuretic peptides exert actions on many key organs involved in blood pressure and water and electrolyte balance. Many of these actions result in a physiological antagonism of angiotensin. To investigate the morphological basis of this interaction, we have mapped the distribution of receptors for atrial natriuretic peptide and angiotensin II in a number of target organs, using 125I-labelled rat atrial natriuretic peptide (99–126) and 125I-labelled [Sar1,Ile8]angiotensin II. In the kidney both atrial natriuretic peptide and angiotensin II receptors were observed overlying glomeruli, vasa recta bundles (high densities), and the outer cortex (moderate density). In the other tissues studied, atrial natriuretic peptide and angiotensin II receptors were codistributed in the adrenal zona glomerulosa, cerebral circumventricular organs including the subfornical organ, organum vasculosum of the lamina terminalis and area postrema, and the external plexiform layer of the olfactory bulb. The concurrent distribution of specific receptors for both peptides at these sites provides the basis for atrial natriuretic peptide to exert a functional antagonism of the actions of angiotensin II on blood pressure and water and electrolyte homeostasis at multiple sites.
5
Buckley, M. G., D. Sethi, N. D. Markandu, G. A. Sagnella, D. R. J. Singer, and G. A. MacGregor. "Plasma concentrations and comparisons of brain natriuretic peptide and atrial natriuretic peptide in normal subjects, cardiac transplant recipients and patients with dialysis-independent or dialysis-dependent chronic renal failure." Clinical Science 83, no. 4 (October 1, 1992): 437–44. http://dx.doi.org/10.1042/cs0830437.
Full textAbstract:
1. We have developed a radioimmunoassay for the measurement of immunoreactive brain natriuretic peptide (1–32) in human plasma. Simultaneous measurements of atrial natriuretic peptide have also been carried out to allow for direct comparison between circulating brain natriuretic peptide and atrial natriuretic peptide. Plasma levels of immunoreactive brain natriuretic peptide (means ± sem) were 1.1 ± 0.1 pmol/l in 36 normal healthy subjects and were significantly elevated in cardiac transplant recipients (18.8 ± 3.9 pmol/l, n = 12) and in patients with dialysis-independent (8.8 ± 1.5 pmol/l, n = 11) or dialysis-dependent (41.6 ± 8.8 pmol/l, n = 14) chronic renal failure. Similarly, in these groups of patients plasma levels of atrial natriuretic peptide were also significantly raised when compared with those in the group of normal healthy subjects. 2. The plasma level of atrial natriuretic peptide was significantly higher than that of brain natriuretic peptide in normal subjects and in patients with dialysis-independent chronic renal failure, with ratios (atrial natriuretic peptide/brain natriuretic peptide) of 2.8 ± 0.2 and 2.2 ± 0.3, respectively. However, in both cardiac transplant recipients and patients on dialysis plasma levels of atrial natriuretic peptide and brain natriuretic peptide were similar, with ratios of 1.3 ± 0.2 and 1.0 ± 0.1, respectively, in these two groups. 3. Plasma levels of brain natriuretic peptide and atrial natriuretic peptide were significantly correlated in the healthy subjects and within each group of patients. When all groups were taken together, there was an overall correlation of 0.90 (P<0.001, n = 73). 4. Patients on dialysis had the highest plasma levels of both brain natriuretic peptide (41.6 ± 8.8 pmol/l, n = 14) and atrial natriuretic peptide (41.3 ± 9.4 pmol/l, n = 14) and the levels of both peptides declined significantly after maintenance haemodialysis. However, the overall percentage decrease in the plasma level of atrial natriuretic peptide (43.6 ± 7.5%) after dialysis was significantly greater than that observed for brain natriuretic peptide (15.9 ± 5.3%, P<0.005). 5. Displacement curves of iodinated atrial natriuretic peptide from bovine adrenal membranes by human atrial natriuretic peptide (99–126) and human brain natriuretic peptide (1–32) gave a median inhibitory concentration of 144 pmol/l for atrial natriuretic peptide and 724.4 pmol/l for brain natriuretic peptide. The cross-reactivity of human brain natriuretic peptide with the atrial natriuretic peptide receptor preparation was 19.5% of that of atrial natriuretic peptide, indicating that human brain natriuretic peptide has a lower binding affinity for the atrial natriuretic peptide receptor/binding site on bovine adrenal membranes. 6. These results suggest that brain natriuretic peptide is co-secreted with atrial natriuretic peptide and may also be an important factor in the adaptive mechanisms to impairment of renal function. However, whether brain natriuretic peptide has an independent and fundamentally important role in man remains to be investigated.
6
Kawakami, Hideo, Hideki Okayama, Mareomi Hamada, and Kunio Hiwada. "Alteration of Atrial Natriuretic Peptide and Brain Natriuretic Peptide Gene Expression Associated with Progression and Regression of Cardiac Hypertrophy in Renovascular Hypertensive Rats." Clinical Science 90, no. 3 (March 1, 1996): 197–204. http://dx.doi.org/10.1042/cs0900197.
Full textAbstract:
1. We assessed the changes of atrial natriuretic peptide and brain natriuretic peptide gene expression associated with progression and regression of cardiac hypertrophy in renovascular hypertensive rats (RHR). 2. Two-kidney, one-clip hypertensive rats (6-week-old male Wistar) were made and studied 6 (RHR-1) and 10 weeks (RHR-2) after the procedure. Regression of cardiac hypertrophy was induced by nephrectomy at 6 weeks after constriction, and the nephrectomized rats were maintained further for 4 weeks (nephrectomized rat: NEP). Sham operation was performed, and the rats were studied after 6 (Sham-1) and 10 weeks (Sham-2). Atrial natriuretic peptide and brain natriuretic peptide gene expression in the left ventricle was analysed by Northern blotting. 3. Plasma atrial natriuretic peptide and brain natriuretic peptide were significantly higher in RHR-1 and RHR-2 than in Sham-1, Sham-2 and NEP. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels in RHR-1 were approximately 7.2-fold and 1.8-fold higher than those in Sham-1, respectively, and the corresponding levels in RHR-2 were 13.0-fold and 2.4-fold higher than those in Sham-2, respectively. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels of NEP were normalized. Levels of atrial natriuretic peptide and brain natriuretic peptide mRNA were well correlated positively with left ventricular weight/body weight ratios. There was a significant positive correlation between the levels of atrial natriuretic peptide and brain natriuretic peptide mRNA (r = 0.86, P<0.01). 4. We conclude that the expression of atrial natriuretic peptide and brain natriuretic peptide genes is regulated in accordance with the degree of myocardial hypertrophy and that the augmented expression of these two natriuretic peptides may play an important role in the maintenance of cardiovascular haemodynamics in renovascular hypertension.
7
Brockhoff, Warnholtz, and Münzel. "Atrial natriuretic peptides – diagnostic and therapeutic potential." Therapeutische Umschau 57, no. 5 (May 1, 2000): 305–12. http://dx.doi.org/10.1024/0040-5930.57.5.305.
Full textAbstract:
Die Familie der natriuretischen Peptide besteht aus insgesamt drei Peptiden, die große Übereinstimmung in Bezug auf die Aminosäuresequenzen und eine Schleife in ihrer Struktur besitzen. Das Atriale Natriuretische Peptid (ANP) und das Brain Natriuretische Peptid (BNP) wirken diuretisch, natriuretisch und vasodilatierend und besitzen wichtige antagonisierende Wirkungen in Bezug auf das Renin-Angiotensin-System. Das CNP hingegen ist weit weniger gut charakterisiert und besitzt im Gegensatz zu ANP und BNP nur vasodilatierende und keine diuretischen Eigenschaften. Die Plasmaspiegel von ANP und BNP sind bei Patienten mit instabiler AP-Symptomatik, akutem Myokardinfarkt und chronischer Herzinsuffizienz erhöht. Aufgrund der bisherigen Untersuchungen besitzt das BNP und nicht das ANP möglicherweise eine gewisse Bedeutung als Prognosefaktor bei Patienten nach Herzinfarkt und bei Patienten mit Herzinsuffizienz. Während die Peptide selbst nur eine geringe Bedeutung in der Therapie der koronaren Herzkrankheit oder Herzinsuffizienz besitzen, scheinen Inhibitoren des ANP-Metabolismus insbesondere in der Kombination mit ACE-Hemmern den klinischen Verlauf positiv beeinflussen zu können.
8
Ekman, Ann-Charlotte, Olli Vakkuri, Olli Vuolteenaho, and Juhani Leppäluoto. "Ethanol Decreases Nocturnal Plasma Levels of Atrial Natriuretic Peptide (ANP 99-126) but Not the N-Terminal Fragment of Pro-Atrial Natriuretic Peptide (ANP 1-98) in Man." Clinical Science 86, no. 3 (March 1, 1994): 285–90. http://dx.doi.org/10.1042/cs0860285.
Full textAbstract:
1. The aim of this study was to elucidate the role of atrial natriuretic peptides in the regulation of water and electrolyte balance after alcohol intake. To this end we measured the plasma concentrations of ethanol, atrial natriuretic peptide 99–126 and the N-terminal fragment of pro-atrial natriuretic peptide (atrial natriuretic peptide 1–98), serum osmolality and serum sodium concentration, and urine output, urine osmolality and urinary sodium excretion for 12 h after administration of ethanol (0, 0.5 and 1.0 g body weight/kg) and placebo drinks to nine healthy subjects according to a double-blind cross-over design. 2. Intake of ethanol (at 19.00–19.45 hours) inhibited the nocturnal increase in the plasma atrial natriuretic peptide 99–126 level dose-dependently (P < 0.05), but had no effect on the plasma atrial natriuretic peptide 1–98 level. Serum osmolality and serum sodium concentration were elevated dose-dependently for 2–5 h after the ethanol intake. Urine volume increased after the higher ethanol dose (net loss of 0.6 litre of water). 3. Since the plasma atrial natriuretic peptide 1–98 level was not changed after ethanol intake, we propose that the alcohol-induced inhibition of the nocturnal rise in the plasma atrial natriuretic peptide 99–126 level is not caused by an inhibition of release, but may rather reflect an increased peripheral elimination of atrial natriuretic peptide 99–126.
9
Lee, Sook Jeong, Sung Zoo Kim, Xun Cui, Suhn Hee Kim, Kyung Sun Lee, Yu Jeong Chung, and Kyung Woo Cho. "C-type natriuretic peptide inhibits ANP secretion and atrial dynamics in perfused atria: NPR-B-cGMP signaling." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 1 (January 1, 2000): H208—H221. http://dx.doi.org/10.1152/ajpheart.2000.278.1.h208.
Full textAbstract:
The purpose of the present experiments was to define the role of C-type natriuretic peptide (CNP) in the regulation of atrial secretion of atrial natriuretic peptide (ANP) and atrial stroke volume. Experiments were performed in perfused beating and nonbeating quiescent atria, single atrial myocytes, and atrial membranes. CNP suppressed in a dose-related fashion the increase in atrial stroke volume and ANP secretion induced by atrial pacing. CNP caused a right shift in the positive relationships between changes in the secretion of ANP and atrial stroke volume or translocation of the extracellular fluid (ECF), which indicates the suppression of atrial myocytic release of ANP into the paracellular space. The effects of CNP on the secretion and contraction were mimicked by 8-bromoguanosine 3′,5′-cyclic monophosphate (8-BrcGMP). CNP increased cGMP production in the perfused atria, and the effects of CNP on the secretion of ANP and atrial dynamics were accentuated by pretreatment with an inhibitor of cGMP phosphodiesterase, zaprinast. An inhibitor of the biological natriuretic peptide receptor (NPR), HS-142-1, attenuated the effects of CNP. The suppression of ANP secretion by CNP and 8-BrcGMP was abolished by a depletion of extracellular Ca2+ in nonbeating atria. Natriuretic peptides increased cGMP production in atrial membranes with a rank order of potency of CNP > BNP > ANP, and the effect was inhibited by HS-142-1. CNP and 8-BrcGMP increased intracellular Ca2+ concentration transients in single atrial myocytes, and mRNAs for CNP and NPR-B were expressed in the rabbit atrium. From these results we conclude that atrial ANP release and stroke volume are controlled by CNP via NPR-B-cGMP mediated signaling, which may in turn act via regulation of intracellular Ca2+.
10
Marumoto, Kazumasa, Mareomi Hamada, and Kunio Hiwada. "Increased Secretion of Atrial and Brain Natriuretic Peptides during Acute Myocardial Ischaemia Induced by Dynamic Exercise in Patients with Angina Pectoris." Clinical Science 88, no. 5 (May 1, 1995): 551–56. http://dx.doi.org/10.1042/cs0880551.
Full textAbstract:
1. This study was conducted to assess the role of atrial and brain natriuretic peptides during acute myocardial ischaemia associated with dynamic exercise. 2. Study subjects consisted of 35 angiographically proven patients with angina pectoris and 35 angiographically normal control subjects. All subjects underwent 201Tl dynamic exercise testing. The presence and localization of the exercise-induced acute myocardial perfusion defect were assessed by 201Tl single-photon emission computed tomography. The severity score was calculated using the early image for quantitative assessment of the acute myocardial perfusion defect. 3. Plasma levels of atrial natriuretic peptide increased from 21.3 ± 3.8 to 72.2 ± 26.7 pg/ml (P < 0.01) in the angina pectoris group, and increased from 19.4 ± 2.4 to 36.4 ± 17.4 pg/ml (P < 0.01) in the control group during dynamic exercise. Plasma levels of brain natriuretic peptide increased from 2.8 ± 0.8 to 6.9 ± 2.6 pg/ml (P < 0.01) in the angina pectoris group, but did not change significantly in the control group (from 2.7 ± 0.7 to 2.9 ± 1.0 pg/ml) during dynamic exercise. At peak exercise, plasma levels of these natriuretic peptides in the angina pectoris group were significantly higher than those in the control group (P < 0.01). 4. At peak exercise, there were correlations between the plasma level of atrial natriuretic peptide and heart rate in both the angina pectoris and control groups (P < 0.01, r = 0.46; P < 0.01, r = 0.51, respectively), but no significant correlations between the plasma level of brain natriuretic peptide and heart rate in either group. The plasma levels of these peptides at peak exercise correlated well with the severity score in the angina pectoris group (atrial natriuretic peptide, r = 0.71, P < 0.01; brain natriuretic peptide, r = 0.69, P < 0.01). 5. The present study showed that plasma levels of atrial and brain natriuretic peptides significantly increased during acute myocardial ischaemia associated with dynamic exercise.
11
Kawai, Yasuaki, and Toshio Ohhashi. "Heterogeneity in responses of isolated monkey arteries and veins to atrial natriuretic peptide." Canadian Journal of Physiology and Pharmacology 67, no. 4 (April 1, 1989): 326–30. http://dx.doi.org/10.1139/y89-053.
Full textAbstract:
Regional differences in responses of isolated monkey arteries and veins to atrial natriuretic peptide were investigated by recording isometric tension. Addition of atrial natriuretic peptide (4 × 10−12 to 4 × 10−8 M) produced a concentration-dependent relaxation in isolated monkey arteries and veins. No significant difference was observed between the responses to rat and human atrial natriuretic peptides. A marked heterogeneity in responses to rat atrial natriuretic peptide, however, was observed in arterial preparations. The decreasing order of the response was as follows: renal > pulmonary > femoral = mesenteric > coronary > middle cerebral > basilar arteries. A heterogeneity in the relaxation produced by atrial natriuretic peptide was also observed in monkey veins. The decreasing order of the response was as follows: pulmonary > mesenteric = portal > femoral > renal = inferior caval veins. On the other hand, 10−5 M sodium nitroprusside caused a maximal relaxation in all monkey arteries and veins used. In the middle cerebral, basilar, and coronary arteries, the relaxant effects of rat atrial natriuretic peptide on KCl-induced contraction were significantly smaller than those on the preparations contracted by an agonist such as prostaglandin F2α. These results suggest that there exist profound regional vasorelaxant selectivities of atrial natriuretic peptide in isolated monkey arteries and veins.Key words: atrial natriuretic peptide, artery, vein, vasodilation, monkey.
12
Tokudome, Takeshi, and Kentaro Otani. "Molecular Mechanism of Blood Pressure Regulation through the Atrial Natriuretic Peptide." Biology 11, no. 9 (September 14, 2022): 1351. http://dx.doi.org/10.3390/biology11091351.
Full textAbstract:
Natriuretic peptides, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP), have cardioprotective effects and regulate blood pressure in mammals. ANP and BNP are hormones secreted from the heart into the bloodstream in response to increased preload and afterload. Both hormones act through natriuretic peptide receptor 1 (NPR1). In contrast, CNP acts through natriuretic peptide receptor 2 (NPR2) and was found to be produced by the vascular endothelium, chondrocytes, and cardiac fibroblasts. Based on its relatively low plasma concentration compared with ANP and BNP, CNP is thought to function as both an autocrine and a paracrine factor in the vasculature, bone, and heart. The cytoplasmic domains of both NPR1 and NPR2 display a guanylate cyclase activity that catalyzes the formation of cyclic GMP. NPR3 lacks this guanylate cyclase activity and is reportedly coupled to Gi-dependent signaling. Recently, we reported that the continuous infusion of the peptide osteocrin, an endogenous ligand of NPR3 secreted by bone and muscle cells, lowered blood pressure in wild-type mice, suggesting that endogenous natriuretic peptides play major roles in the regulation of blood pressure. Neprilysin is a neutral endopeptidase that degrades several vasoactive peptides, including natriuretic peptides. The increased worldwide clinical use of the angiotensin receptor-neprilysin inhibitor for the treatment of chronic heart failure has brought renewed attention to the physiological effects of natriuretic peptides. In this review, we provide an overview of the discovery of ANP and its translational research. We also highlight our recent findings on the blood pressure regulatory effects of ANP, focusing on its molecular mechanisms.
13
Geelhoed, Bastiaan, Christin S. Börschel, Teemu Niiranen, Tarja Palosaari, Aki S. Havulinna, Césaire J. K. Fouodo, Markus O. Scheinhardt, et al. "Assessment of causality of natriuretic peptides and atrial fibrillation and heart failure: a Mendelian randomization study in the FINRISK cohort." EP Europace 22, no. 10 (August 23, 2020): 1463–69. http://dx.doi.org/10.1093/europace/euaa158.
Full textAbstract:
Abstract Aims Natriuretic peptides are extensively studied biomarkers for atrial fibrillation (AF) and heart failure (HF). Their role in the pathogenesis of both diseases is not entirely understood and previous studies several single-nucleotide polymorphisms (SNPs) at the NPPA-NPPB locus associated with natriuretic peptides have been identified. We investigated the causal relationship between natriuretic peptides and AF as well as HF using a Mendelian randomization approach. Methods and results N-terminal pro B-type natriuretic peptide (NT-proBNP) (N = 6669), B-type natriuretic peptide (BNP) (N = 6674), and mid-regional pro atrial natriuretic peptide (MR-proANP) (N = 6813) were measured in the FINRISK 1997 cohort. N = 30 common SNPs related to NT-proBNP, BNP, and MR-proANP were selected from studies. We performed six Mendelian randomizations for all three natriuretic peptide biomarkers and for both outcomes, AF and HF, separately. Polygenic risk scores (PRSs) based on multiple SNPs were used as genetic instrumental variable in Mendelian randomizations. Polygenic risk scores were significantly associated with the three natriuretic peptides. Polygenic risk scores were not significantly associated with incident AF nor HF. Most cardiovascular risk factors showed significant confounding percentages, but no association with PRS. A causal relation except for small causal betas is unlikely. Conclusion In our Mendelian randomization approach, we confirmed an association between common genetic variation at the NPPA-NPPB locus and natriuretic peptides. A strong causal relationship between natriuretic peptides and incidence of AF as well as HF at the community-level was ruled out. Therapeutic approaches targeting natriuretic peptides will therefore very likely work through indirect mechanisms.
14
LAINCHBURY, J. G., M. G. NICHOLLS, E. A. ESPINER, H. IKRAM, T. G. YANDLE, and A. M. RICHARDS. "Regional plasma levels of cardiac peptides and their response to acute neutral endopeptidase inhibition in man." Clinical Science 95, no. 5 (November 1, 1998): 547–55. http://dx.doi.org/10.1042/cs0950547.
Full textAbstract:
1.The cardiac natriuretic peptides, atrial natriuretic peptide and brain natriuretic peptide, are degraded via clearance receptors and the enzyme neutral endopeptidase (EC 3.4.24.11). We studied the regional plasma concentrations of these peptides and their response to acute neutral endopeptidase inhibition in a consecutive series of patients with a broad spectrum of severity of cardiac dysfunction who were undergoing diagnostic right and left heart catheterization (24 patients, mean age 62.6 years). 2.Baseline blood samples were obtained for hormone analysis from femoral artery, femoral vein, renal vein, hepatic vein, superior vena cava, coronary sinus and pulmonary artery, and initial haemodynamic measurements were made. Twelve patients then received a neutral endopeptidase inhibitor (SCH 32615, 200 ;mg intravenously) and 12 received vehicle alone. The cardiac catheterization procedure was then completed and haemodynamic and hormone measurements were repeated. 3.Haemodynamic status was similar at baseline in both groups, and at repeated measurement (post-procedure after placebo or active drugs) haemodynamic variables were not significantly different from baseline values. Plasma levels of atrial and brain natriuretic peptides exhibited an arteriovenous increment (344% and 124% respectively) across the heart (femoral artery to coronary sinus) and decrement (by 28–54% and 9–16% respectively) across all other tissue beds (P< 0.05 for all) except the lung (no change). Final levels of atrial natriuretic peptide rose above initial levels at all sites in both groups (P< 0.05) except coronary sinus levels in the vehicle group (no change). The increase was consistently greater in the inhibitor group at all sites (P< 0.05 versus placebo). Levels of brain natriuretic peptide rose at all sites in the inhibitor group only (P< 0.05). The transcardiac step-up in atrial natriuretic peptide was markedly augmented after the administration of neutral endopeptidase inhibitor. Other tissue gradients were not significantly altered by neutral endopeptidase inhibitor. 4.Atrial and brain natriuretic peptides in plasma are degraded by a number of tissues, and respond differently to cardiac catheterization. Neutral endopeptidase has a significant role in determining plasma levels of natriuretic peptides, in part perhaps by influencing the amount of intact peptide reaching the circulation after secretion from the heart.
15
Ogawa, Tsuneo, and Adolfo J. de Bold. "The heart as an endocrine organ." Endocrine Connections 3, no. 2 (June 2014): R31—R44. http://dx.doi.org/10.1530/ec-14-0012.
Full textAbstract:
The concept of the heart as an endocrine organ arises from the observation that the atrial cardiomyocytes in the mammalian heart display a phenotype that is partly that of endocrine cells. Investigations carried out between 1971 and 1983 characterised, by virtue of its natriuretic properties, a polypeptide referred to atrial natriuretic factor (ANF). Another polypeptide isolated from brain in 1988, brain natriuretic peptide (BNP), was subsequently characterised as a second hormone produced by the mammalian heart atria. These peptides were associated with the maintenance of extracellular fluid volume and blood pressure. Later work demonstrated a plethora of other properties for ANF and BNP, now designated cardiac natriuretic peptides (cNPs). In addition to the cNPs, other polypeptide hormones are expressed in the heart that likely act upon the myocardium in a paracrine or autocrine fashion. These include the C-type natriuretic peptide, adrenomedullin, proadrenomedullin N-terminal peptide and endothelin-1. Expression and secretion of ANF and BNP are increased in various cardiovascular pathologies and their levels in blood are used in the diagnosis and prognosis of cardiovascular disease. In addition, therapeutic uses for these peptides or related substances have been found. In all, the discovery of the endocrine heart provided a shift from the classical functional paradigm of the heart that regarded this organ solely as a blood pump to one that regards this organ as self-regulating its workload humorally and that also influences the function of several other organs that control cardiovascular function.
16
Flynn, T. Geoffrey. "The elucidation of the structure of atrial natriuretic factor, a new peptide hormone." Canadian Journal of Physiology and Pharmacology 65, no. 10 (October 1, 1987): 2013–20. http://dx.doi.org/10.1139/y87-315.
Full textAbstract:
The benchmark experiments of Adolfo de Bold and Harald Sonnenberg revealed that heart atria contained a substance or substances (atrial natriuretic factor) which when injected into rats caused a profound diuresis, natriuresis, and fall in blood pressure. Acid extraction and purification of atrial natriuretic factor resulted initially in the purification of a low molecular weight peptide containing a disulfide bond. This peptide was named cardionatrin I. Amino acid sequencing of less than 1 nmol of cardionatrin I revealed it to be a 28-residue peptide with the following structure: [Formula: see text]The position of the disulfide bond was verified by a radioactive method. From the sequence of complementary DNA for atrial natriuretic factor, the 28-residue peptide was shown to be the C-terminal portion of a larger protein called pro-atrial natriuretic factor. The discovery and characterization of atrial natriuretic factor substantiated the idea that the heart atria serve in an endocrine capacity.
17
Song, H., J. Papadimitriou, C. Drachenberg, M. R. Weir, and C. Wei. "Enhancement of Natriuretic Peptides in Rejected Human Renal Graft." Microscopy and Microanalysis 6, S2 (August 2000): 602–3. http://dx.doi.org/10.1017/s1431927600035509.
Full textAbstract:
Natriuretic peptides include atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP). ANP, BNP and CNP are structure related but genetic distinct 1 natriuretic peptide family. ANP and BNP are cardiac cell origin and CNP are endothelial cell and kidney origin. Natriuretic peptides have potent vasoactive and natriuretic actions through generation of cGMP. On the other hand, renal graft rejection is major problem after kidney transplantation with severe renal damage and renal vasoconstriction. We hypothesized that renal tissue level of natriuretic peptides increase in renal graft rejection through compensatory mechanism. Therefore, the present study was designed to determine the expression of natriuretic peptides by immunohistochemical staining (IHCS) in human renal tissue with rejection and compare with normal renal tissue.Human renal biopsy (n=5) were obtained after kidney transplantation with mild and moderate renal rejection. Normal kidney biopsy was obtained during nephrectomy. ANP, BNP and CNP levels in renal tissue were determined by IHCS.
18
Vesely, D. L., S. Chiou, M. A. Douglass, M. T. McCormick, G. Rodriguez-Paz, and D. D. Schocken. "Kaliuretic peptide and long acting natriuretic peptide as well as atrial natriuretic factor inhibit aldosterone secretion." Journal of Endocrinology 146, no. 3 (September 1995): 373–80. http://dx.doi.org/10.1677/joe.0.1460373.
Full textAbstract:
Abstract The present investigation was designed to determine whether atrial natriuretic peptides consisting of amino acids 1–30 (long acting natriuretic peptide), 31–67 (vessel dilator) and 79–98 (kaliuretic peptide) as well as 99–126 (atrial natriuretic factor (ANF)) of the 126 amino acid ANF prohormone inhibit aldosterone secretion. Thirty healthy human subjects were studied following infusion of 100 ng/kg body weight/min for 60 min of each of the respective peptides. Kaliuretic peptide decreased plasma aldosterone concentration by the greatest amount (6-fold) and plasma aldosterone was still significantly decreased (P<0·001) three hours after stopping the infusion. In contrast, within 30 min of cessation of the ANF infusion, plasma aldosterone levels had returned to pre-infusion values. Long acting natriuretic peptide also significantly (P<0·01) decreased plasma aldosterone levels which remained significantly (P<0·001) decreased 3 h after cessation of infusion. Vessel dilator did not decrease plasma aldosterone levels. Kaliuretic peptide, ANF and long acting natriuretic peptide also decreased (P<0·01) urinary aldosterone concentrations. None of these peptides changed the plasma potassium concentration. We conclude that two new peptide hormones (long acting natriuretic peptide and kaliuretic peptide) inhibit aldosterone secretion. The length of time that aldosterone secretion is inhibited following kaliuretic peptide and long acting natriuretic peptide infusion is significantly longer (P<0·001) than following ANF infusion. Journal of Endocrinology (1995) 146, 373–380
19
Renkin, EM, and VL Tucker. "Atrial Natriuretic Peptide as a Regulator of Transvascular Fluid Balance." Physiology 11, no. 3 (June 1, 1996): 138–43. http://dx.doi.org/10.1152/physiologyonline.1996.11.3.138.
Full textAbstract:
Unlike other natriuretics, which act via the kidneys to reduce interstitial fluid volume with little change in plasma volume, atrial natriuretic peptide has important extrarenal actions that enable it to reduce plasma volume preferentially.
20
Hamada, Mareomi, Yuji Shigematsu, Hideo Kawakami, Naoto Minamino, Kenji Kangawa, Hisayuki Matsuo, and Kunio Hiwada. "Increased Plasma Levels of Adrenomedullin in Patients with Hypertrophic Cardiomyopathy: Its Relation to Endothelin-1, Natriuretic Peptides and Noradrenaline." Clinical Science 94, no. 1 (January 1, 1998): 21–28. http://dx.doi.org/10.1042/cs0940021.
Full textAbstract:
1. The aim of this study was to elucidate the pathophysiological role of adrenomedullin and the relation between adrenomedullin and other hormones in patients with hypertrophic cardiomyopathy. 2. Fourteen patients with hypertrophic obstructive cardiomyopathy (HOCM), 26 patients with hypertrophic non-obstructive cardiomyopathy (HNCM) and 14 normal control subjects participated in this study. Radioimmunoassay for plasma adrenomedullin concentration was performed with adrenomedullin-M antibody. Plasma levels of endothelin-1, atrial and brain natriuretic peptides and noradrenaline were also measured. 3. Plasma levels of adrenomedullin were higher in patients with hypertrophic cardiomyopathy (8.43 ± 3.73 pmol/l) than in normal controls (5.24 ± 0.44 pmol/l, P < 0.005). There was no significant difference between HOCM and HNCM patients. There was a weak correlation between plasma levels of adrenomedullin and total 12-lead QRS voltage in patients with hypertrophic cardiomyopathy (r = 0323, P < 0.05) 4. Plasma levels of endothelin-1, atrial and brain natriuretic peptides were higher in hypertrophic cardiomyopathy than in normal controls. Endothelin-1 showed no significant difference between HOCM and HNCM patients, but atrial and brain natriuretic peptides were higher in HOCM than in HNCM patients. There was a positive correlation between plasma levels of adrenomedullin and endothelin-1 (r = 0.575, P < 0.0001), but no correlation between plasma levels of adrenomedullin and atrial natriuretic peptide, brain natriuretic peptide and noradrenaline. 5. Our results indicate that adrenomedullin may play an important role to maintain haemodynamics in patients with hypertrophic cardiomyopathy, and its action may be related to endothelin-1 but independent of atrial natriuretic peptide, brain natriuretic peptide and noradrenaline.
21
Kitamura, Hiroaki, Daisuke Nakano, Yoshiharu Sawanobori, Takehiko Asaga, Hideki Yokoi, Motoko Yanagita, Masashi Mukoyama, et al. "Guanylyl Cyclase A in Both Renal Proximal Tubular and Vascular Endothelial Cells Protects the Kidney against Acute Injury in Rodent Experimental Endotoxemia Models." Anesthesiology 129, no. 2 (August 1, 2018): 296–310. http://dx.doi.org/10.1097/aln.0000000000002214.
Full textAbstract:
Abstract What We Already Know about This Topic What This Article Tells Us That Is New Background Natriuretic peptides are used, based on empirical observations, in intensive care units as antioliguric treatments. We hypothesized that natriuretic peptides prevent lipopolysaccharide-induced oliguria by activating guanylyl cyclase A, a receptor for natriuretic peptides, in proximal tubules and endothelial cells. Methods Normal Sprague-Dawley rats and mice lacking guanylyl cyclase A in either endothelial cells or proximal tubular cells were challenged with lipopolysaccharide and assessed for oliguria and intratubular flow rate by intravital imaging with multiphoton microscopy. Results Recombinant atrial natriuretic peptide efficiently improved urine volume without changing blood pressure after lipopolysaccharide challenge in rats (urine volume at 4 h, lipopolysaccharide: 0.6 ± 0.3 ml · kg−1 · h−1; lipopolysaccharide + fluid resuscitation: 4.6 ± 2.0 ml · kg−1 · h−1; lipopolysaccharide + fluid resuscitation + atrial natriuretic peptide: 9.0 ± 4.8 ml · kg−1 · h−1; mean ± SD; n = 5 per group). Lipopolysaccharide decreased glomerular filtration rate and slowed intraproximal tubular flow rate, as measured by in vivo imaging. Fluid resuscitation restored glomerular filtration rate but not tubular flow rate. Adding atrial natriuretic peptide to fluid resuscitation improved both glomerular filtration rate and tubular flow rate. Mice lacking guanylyl cyclase A in either proximal tubules or endothelium demonstrated less improvement of tubular flow rate when treated with atrial natriuretic peptide, compared with control mice. Deletion of endothelial, but not proximal tubular, guanylyl cyclase A augmented the reduction of glomerular filtration rate by lipopolysaccharide. Conclusions Both endogenous and exogenous natriuretic peptides prevent lipopolysaccharide-induced oliguria by activating guanylyl cyclase A in proximal tubules and endothelial cells.
22
BORGESON, Daniel D., Tracy L. STEVENS, Denise M. HEUBLEIN, Yuzuru MATSUDA, and John C. BURNETT. "Activation of myocardial and renal natriuretic peptides during acute intravascular volume overload in dogs: functional cardiorenal responses to receptor antagonism." Clinical Science 95, no. 2 (August 1, 1998): 195–202. http://dx.doi.org/10.1042/cs0950195.
Full textAbstract:
1.A family of structurally related but genetically distinct natriuretic peptides exist which include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) of myocardial cell origin and C-type natriuretic peptide (CNP) of endothelial and renal epithelial cell origin. All three exert actions via cGMP, with ANP and BNP functioning via the natriuretic peptide A receptor and CNP via the natriuretic peptide B receptor. 2.Circulating and urinary natriuretic peptides were determined in response to acute intravascular volume overload (AVO). Additionally, their functional role in cardiorenal regulation during AVO was investigated by utilizing the natriuretic peptide receptor antagonist HS-142-1. Control (n = 5) and study dogs (HS-142-1, n = 9) underwent AVO with normal saline equal to 10% of body weight over 1 ;h. Both groups demonstrated similar significant increases in right atrial pressure, pulmonary capillary wedge pressure, pulmonary artery pressure and cardiac output. Circulating ANP paralleled increases in right atrial pressure and pulmonary capillary wedge pressure, with no changes in plasma BNP or CNP. At peak AVO, urinary CNP excretion was increased compared with baseline (7.0±4.2 versus 62±8.0 ;pg/min, P< 0.05). 3.In the HS-142-1-treated group, plasma cGMP was decreased compared with the control group (9.6±1.1 to 5.0±1.2 ;pmol/ml, P< 0.05). A significant attenuation of natriuresis (566±91 versus 1241±198 ;μEq/min, P< 0.05) and diuresis (4.8±0.7 versus 10.1±2.0 ;ml/min, P< 0.05) was also observed at peak AVO in the HS-142-1 treated group. 4.These findings support differential and selective responses of the three natriuretic peptides to AVO, in which plasma ANP and urinary CNP are markers for AVO. Secondly, these studies confirm the role of ANP and CNP but not BNP in the natriuretic and diuretic response to acute volume overload.
23
Eindhoven, Jannet A., Annemien E. van den Bosch, Eric Boersma, and Jolien W. Roos-Hesselink. "The usefulness of brain natriuretic peptide in simple congenital heart disease – a systematic review." Cardiology in the Young 23, no. 3 (September 20, 2012): 315–24. http://dx.doi.org/10.1017/s1047951112001205.
Full textAbstract:
AbstractBrain natriuretic peptide and N-terminal pro-brain natriuretic peptide are two well-established markers for cardiac failure in acquired heart disease. Nevertheless, the clinical utility of these markers in patients with congenital heart disease remains unclear. Therefore, the aim of this study was to evaluate the diagnostic and prognostic value of these markers in patients with congenital heart disease. A PubMed and EMBASE literature search was executed with focus on the most common simple congenital heart defects, atrial septal defect and ventricular septal defect. Data on brain natriuretic peptide measurement, cardiac function parameters, and follow-up were collected. In patients with atrial or ventricular septal defect, brain natriuretic peptide levels were mildly increased when compared with healthy age-matched controls. Shunt severity and pulmonary artery pressure correlated strongly with natriuretic peptide levels. A clear association between brain natriuretic peptide and functional class was demonstrated. After closure of the defect, a rise in brain natriuretic peptide levels in the first hours to days was observed. After longer follow-up, natriuretic peptide levels decreased and became comparable to pre-procedural values. In conclusion, this systematic review shows that brain natriuretic peptide levels are mildly increased in patients with unrepaired and repaired atrial or ventricular septal defect. Brain natriuretic peptide measurement might be a useful additional tool in the diagnostic work-up of patients with atrial or ventricular septal defect. Further investigation in a larger, prospective study with long-term follow-up is warranted to elucidate the true prognostic value of natriuretic peptides in patients with simple congenital heart disease.
24
Buckley, M. G., N. D. Markandu, G. A. Sagnella, and G. A. MacGregor. "N-Terminal Atrial Natriuretic Peptide and Atrial Natriuretic Peptide in Human Plasma: Investigation of Plasma Levels and Molecular Circulating Form(s) Using Radioimmunoassays for Pro-Atrial Natriuretic Peptide (31–67), Pro-Atrial Natriuretic Peptide (1–30) and Atrial Natriuretic Peptide (99–126)." Clinical Science 87, no. 3 (September 1, 1994): 311–17. http://dx.doi.org/10.1042/cs0870311.
Full textAbstract:
1. The aim of this study was to determine plasma levels of N-terminal atrial natriuretic peptide and atrial natriuretic peptide in normal subjects and in patients with essential hypertension, cardiac transplant and chronic renal failure, using radioimmunoassays directed towards the mid-portion pro-atrial natriuretic peptide (31-67) and pro-atrial natriuretic peptide (1-30) of the N-terminal atrial natriuretic peptide and atrial natriuretic peptide (99-126). The circulating form(s) of the immunoreactive N-terminal atrial natriuretic peptide in plasma extracts has been investigated using all three radioimmunoassays by means of gel filtration chromatography to further clarify the major immunoreactive molecular circulating form(s) of N-terminal atrial natriuretic peptide in man. 2. The plasma level (mean ± SEM) of N-terminal pro-atrial natriuretic peptide (31-67) in the normal subjects was 547.2 ± 32.7 pg/ml (n = 36) and was significantly elevated in patients with essential hypertension (730.2 ± 72.3 pg/ml, P < 0.025, n = 39), in cardiac transplant recipients (3214.0 ± 432.2 pg/ml, P < 0.001, n = 9) and in patients with chronic renal failure (3571.8 ± 474.1 pg/ml, P < 0.001, n = 11). Plasma levels of N-terminal pro-atrial natriuretic peptide (1-30) and atrial natriuretic peptide were similarly elevated in the same patient groups when compared with the mean plasma values in the normal subjects. 3. There were positive associations between pro-atrial natriuretic peptide (31-67) and atrial natriuretic peptide, pro-atrial natriuretic peptide (31-67) and pro-atrial natriuretic peptide (1-30) and between pro-atrial natriuretic peptide (1-30) and atrial natriuretic peptide in the normal subjects, hypertensive patients, cardiac transplant recipients and patients with chronic renal failure. The correlation coefficient for all groups taken together was 0.86 (P < 0.001. n = 95) for pro-atrial natriuretic peptide (31-67) and atrial natriuretic peptide, 0.93 (P < 0.001, n = 95) for pro-atrial natriuretic peptide (31-67) and pro-atrial natriuretic peptide (1-30), and 0.82 (p < 0.001, n = 95) for pro-atrial natriuretic peptide (1-30) and atrial natriuretic peptide. 4. Gel filtration of extracted plasma from cardiac transplant patients and patients with chronic renal failure indicated a single peak of immunoreactivity for N-terminal atrial natriuretic peptide using both the pro-atrial natriuretic peptide (31-67) and pro-atrial natriuretic peptide (1-30) radioimmunoassays, suggesting a major single high-molecular-mass circulating immunoreactive N-terminal atrial natriuretic peptide, probably pro-atrial natriuretic peptide (1-98). Atrial natriuretic peptide immunoreactivity, as measured by the radioimmunoassay for atrial natriuretic peptide (99-126), showed a separate and distinct peak from that of the N-terminal atrial natriuretic peptide, which co-eluted with the synthetic human standard atrial natriuretic peptide (99-126). 5. These results show that immunoreactive N-terminal atrial natriuretic peptide and atrial natriuretic peptide are elevated in patients with essential hypertension, in cardiac transplant recipients and in patients with chronic renal failure. The major immunoreactive form of N-terminal atrial natriuretic peptide cross-reacting in both the pro-atrial natriuretic peptide (31-67) and pro-atrial natriuretic peptide (1-30) radioimmunoassays is of a high molecular mass, probably pro-atrial natriuretic peptide (1-98). Since pro-atrial natriuretic peptide (1-98) is unlikely to cross-react identically with antibodies for pro-atrial natriuretic peptide (31-67) or pro-atrial natriuretic peptide (1-30), this could account for the differences in plasma levels obtained by the assays for pro-atrial natriuretic peptide (31-67) and pro-atrial natriuretic peptide (1-30).
25
Dajak, Marijana, Svetlana Ignjatovic, and Nada Majkic-Singh. "The significance of determination of heart natriuretic peptides in heart insufficiency." Jugoslovenska medicinska biohemija 22, no. 4 (2003): 311–17. http://dx.doi.org/10.2298/jmh0304311d.
Full textAbstract:
Heart natriuretic peptides, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) act as key regulators of homeostasis of body fluids volume and blood pressure, by decreasing salt excess and water retention, and by inhibiting intensive action of sympathetic nervous system and secretion of vasoconstrictor hormones. Plasma ANP, N-terminal pro-atrial natriuretic peptide (NT-proANP), BNP and N-terminal pro-brain natriuretic peptide (NT-proBNP) concentrations are considerably increased in heart insufficiency. Intracardiac pressure and atrial and ventricular wall tension are the prime regulators of natriuretic peptides release from the heart. ANP primarily reflects atrial, and BNP ventricular overload. The in vitro stabilities of NT-proANP, BNP and NT-proBNP in EDTA whole blood are sufficient for routine determination. Specific immunochemical tests with acceptable precision are commercially available. However, the determinations are not standardized, which makes difficulties during the comparation of results gained by tests from different manufactures. BNP and NT-proBNP are in relation to ANP and NT-proANP, better diagnostic and prognostic markers of heart insufficiency. BNP measurement is useful for screening in high-risk population. BNP has an excellent negative predictive value for left ventricular dysfunction. It is also suitable for screening hypertensive patients for the discovery of hypertrophy or/and dysfunction of left ventriculy, as well as for risk assessment during the subacute phase of acute myocardial infarction. BNP and NT-proBNP measurement is also useful for treatment guidance and optimization of therapy in heart insufficiency. However, BNP determination cannot replace echocardiography or similar techniques, because these methods provide different information. Thus for the cardiologists natriuretic peptides determination is useful addition to the standard clinical investigation of patients with ventricular dysfunction.
26
Siebert, Janusz, Łukasz Lewicki, Jolanta Myśliwska, Monika Młotkowska, and Jan Rogowski. "Scal atrial natriuretic peptide gene polymorphisms and their possible association with postoperative atrial fibrillation – a preliminary report." Archives of Medical Science 3 (2017): 568–74. http://dx.doi.org/10.5114/aoms.2016.58270.
Full text
27
Speake, P. F., S. C. Pirie, J. D. Kibble, A. Muneer, D. Taylor, S. Birring, and R. Green. "Dose-Response Effects of Adrenergic and Cholinergic Stimulation on Atrial Natriuretic Peptide Secretion from Beating Isolated Guinea-Pig Atria." Clinical Science 85, no. 1 (July 1, 1993): 5–12. http://dx.doi.org/10.1042/cs0850005.
Full textAbstract:
1. The possible role of autonomic neurotransmitters in atrial natriuretic peptide secretion was investigated using spontaneously beating guinea-pig atria in vitro. Dose responses were determined for adrenaline, noradrenaline and acetylcholine and the selective α- and β-adrenoceptor agonists phenylephrine and isoprenaline, respectively. Adrenoceptor effects were further studied using the selective α- and β-adrenoceptor antagonists prazosin and propranolol, respectively, in conjunction with maximal adrenaline challenge. Results for rate and force of contraction and atrial natriuretic peptide secretion are expressed as a ratio (mean ± SEM) of a 15 min treatment period (stage 2) to a corresponding pretreatment period (stage 1). 2. Adrenaline and noradrenaline caused dose-dependent increases in the rate and force of contraction and in atrial natriuretic peptide secretion with a peak secretory response at 2 × 10−6 mol/l of 1.54 ± 0.08 (P <0.01) and 1.34 ± 0.08 (P <0.01) for adrenaline and noradrenaline, respectively. Acetylcholine decreased the rate and force of contraction, and ANP secretion was reduced to 0.47 ± 0.06 at 3 × 10−5 mol/l (P <0.01). Isoprenaline increased the rate and force of contraction and atrial natriuretic peptide secretion with a peak secretory response of 152 ± 0.22 at 2 × 10−6 mol/l (P <0.01). Phenylephrine increased the force but had no effect on the rate of contraction, and stimulated atrial natriuretic peptide secretion to 1.13 ± 0.09 at 2 × 10−5 mol/l (P <0.05). After both α- and β-adrenoceptor blockade, adrenaline was still able to significantly stimulate atrial natriuretic peptide secretion and positive inotropy. There was no chronotropic effect of adrenaline in the presence of propranolol. Simultaneous α- and β-adrenoceptor blockade inhibited all the effects of adrenaline. 3. A significant correlation was observed between the absolute change in rate of contraction and the absolute change in atrial natriuretic peptide secretion upon stimulation with each of the drugs (r = 0.63, P < 0.001). A similar relationship between developed tension and atrial natriuretic peptide secretion could not be demonstrated. 4. In conclusion, secretion of atrial natriuretic peptide from guinea-pig atria was stimulated by adrenergic and inhibited by cholinergic agonists. The adrenergic response was mediated by both α- and β-adrenoceptor stimulation. The observed changes in the rate of contraction showed a significant correlation with atrial natriuretic peptide secretion.
28
Hagiwara, H., A. Inoue, A. Yamaguchi, S. Yokose, M. Furuya, S. Tanaka, and S. Hirose. "cGMP produced in response to ANP and CNP regulates proliferation and differentiation of osteoblastic cells." American Journal of Physiology-Cell Physiology 270, no. 5 (May 1, 1996): C1311—C1318. http://dx.doi.org/10.1152/ajpcell.1996.270.5.c1311.
Full textAbstract:
The effects of natriuretic peptides on the proliferation and differentiation of osteoblast-like cells from rat calvariae were examined. Natriuretic peptides are physiological agonists that activate receptor guanylate cyclases, namely, natriuretic peptide receptor (NPR)-A and NPR-B. Exposure of cells to atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP) resulted in large increases in the rate of intracellular production of guanosine 3',5'-cyclic monophosphate (cGMP). Moreover, CNP-like immunoreactivity was detected in the conditioned medium from osteoblast-like cells, while ANP was undetectable. In cells exposed to natriuretic peptides, a dose-dependent reduction in the rate of DNA synthesis was observed. Natriuretic peptides also stimulated the activity of alkaline phosphatase (ALPase) and the expression of mRNA for ALPase and osteocalcin and the mineralization of nodules by the cultured cells. These results could be reproduced by treating cells with 8-bromo-cGMP. Endothelin-1, whose physiological functions are the opposite of those of natriuretic peptides, decreased the ALPase activity and the mineralization of nodules. In the present study, natriuretic peptides were demonstrated to promote bone formation via the action of cGMP in a signal-transduction pathway mediated by specific receptors in osteoblast-like cells.
29
Nakagawa, Hitoshi, and Yoshihiko Saito. "Roles of Natriuretic Peptides and the Significance of Neprilysin in Cardiovascular Diseases." Biology 11, no. 7 (July 6, 2022): 1017. http://dx.doi.org/10.3390/biology11071017.
Full textAbstract:
Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) activate the guanylyl cyclase A receptor (GC-A), which synthesizes the second messenger cGMP in a wide variety of tissues and cells. C-type natriuretic peptide (CNP) activates the cGMP-producing guanylyl cyclase B receptor (GC-B) in chondrocytes, endothelial cells, and possibly smooth muscle cells, cardiomyocytes, and cardiac fibroblasts. The development of genetically modified mice has helped elucidate the physiological roles of natriuretic peptides via GC-A or GC-B. These include the hormonal effects of ANP/BNP in the vasculature, autocrine effects of ANP/BNP in cardiomyocytes, and paracrine effects of CNP in the vasculature and cardiomyocytes. Neprilysin (NEP) is a transmembrane neutral endopeptidase that degrades the three natriuretic peptides. Recently, mice overexpressing NEP, specifically in cardiomyocytes, revealed that local cardiac NEP plays a vital role in regulating natriuretic peptides in the heart tissue. Since NEP inhibition is a clinically accepted approach for heart failure treatment, the physiological roles of natriuretic peptides have regained attention. This article focuses on the physiological roles of natriuretic peptides elucidated in mice with GC-A or GC-B deletion, the significance of NEP in natriuretic peptide metabolism, and the long-term effects of angiotensin receptor-neprilysin inhibitor (ARNI) on cardiovascular diseases.
30
Potter, Lincoln R., Sarah Abbey-Hosch, and Deborah M. Dickey. "Natriuretic Peptides, Their Receptors, and Cyclic Guanosine Monophosphate-Dependent Signaling Functions." Endocrine Reviews 27, no. 1 (November 16, 2005): 47–72. http://dx.doi.org/10.1210/er.2005-0014.
Full textAbstract:
Natriuretic peptides are a family of structurally related but genetically distinct hormones/paracrine factors that regulate blood volume, blood pressure, ventricular hypertrophy, pulmonary hypertension, fat metabolism, and long bone growth. The mammalian members are atrial natriuretic peptide, B-type natriuretic peptide, C-type natriuretic peptide, and possibly osteocrin/musclin. Three single membrane-spanning natriuretic peptide receptors (NPRs) have been identified. Two, NPR-A/GC-A/NPR1 and NPR-B/GC-B/NPR2, are transmembrane guanylyl cyclases, enzymes that catalyze the synthesis of cGMP. One, NPR-C/NPR3, lacks intrinsic enzymatic activity and controls the local concentrations of natriuretic peptides through constitutive receptor-mediated internalization and degradation. Single allele-inactivating mutations in the promoter of human NPR-A are associated with hypertension and heart failure, whereas homozygous inactivating mutations in human NPR-B cause a form of short-limbed dwarfism known as acromesomelic dysplasia type Maroteaux. The physiological effects of natriuretic peptides are elicited through three classes of cGMP binding proteins: cGMP-dependent protein kinases, cGMP-regulated phosphodiesterases, and cyclic nucleotide-gated ion channels. In this comprehensive review, the structure, function, regulation, and biological consequences of natriuretic peptides and their associated signaling proteins are described.
31
Pianca, Eduardo Vitor, Walter Krause Neto, Alexandre Sabbag da Silva, Eliane Florencio Gama, and Romeu Rodrigues de Souza. "ACUTE EFFECT OF DIFFERENT TYPES OF EXERCISE ON NATRIURETIC PEPTIDES OF WISTAR RATS." Revista Brasileira de Medicina do Esporte 25, no. 4 (August 2019): 310–15. http://dx.doi.org/10.1590/1517-869220192504214335.
Full textAbstract:
ABSTRACT Introduction: The study of the effects of different types of physical exercise on cardiovascular physiology is increasing in the literature. The many mechanisms of hemodynamic control include the atrial release of natriuretic peptides. Although extensive evidence demonstrates their acute effects and the increase in their plasma concentration, it is not known whether both atria respond in a similar way to both types of natriuretic peptide in response to different types of exercise. Objective: To compare the acute responses of different exercise types in the atrial (ANP) and brain (BNP) natriuretic peptides of both atrial cardiomyocytes of Wistar rats. Methods: Animals were divided into control (CG), aerobic (AG), resistance (RG) and combined (ARG). The RG performed six climbs, with a load equivalent to 60% of body weight. The AG ran on a treadmill at a speed of 12m/min for 60 minutes. The ARG exercise consisted of three consecutive ladder climbs, followed by 30 minutes of running. Results: First, the right atrium released more ANP and BNP during all types of exercise; second, the resistance exercise released the most ANP and BNP in both atria; third, in the right atrium, aerobic and combined workouts released more small and medium ANP granules while resistance exercise released larger BNP granules; and fourth, in the left atrium, aerobic exercise released more ANP granules while resistance and combined exercise released larger ANP and BNP granules. Conclusion: All types of exercise induce partial release of natriuretic peptide granules, with greater response to resistance exercise. Furthermore, a particular and different response could be seen in both types of atria in the release of ANP and BNP. Level of evidence II; Therapeutic studies - Investigation of treatment results.
32
RADEMAKER, Miriam T., Chris J. CHARLES, Eric A. ESPINER, Chris M. FRAMPTON, M. Gary NICHOLLS, and A. Mark RICHARDS. "Combined inhibition of angiotensin II and endothelin suppresses the brain natriuretic peptide response to developing heart failure." Clinical Science 106, no. 6 (June 1, 2004): 569–76. http://dx.doi.org/10.1042/cs20030366.
Full textAbstract:
Blockade of AngII (angiotensin II) and ET (endothelin)-1, established and potential therapeutic strategies respectively, for heart failure, may have an adverse effect on the cardiac secretion of the natriuretic peptides, hormones with actions beneficial in this disease. The present study investigates the roles of AngII and ET-1 in regulating the stretch-induced release of the natriuretic peptides during the development of heart failure. On seven separate days, eight sheep underwent incremental left ventricular pacing (155, 190 and 225 beats/min for 90 min each) with concurrent infusions of a vehicle control, AngII, ET-1, AngII+ET-1, losartan [AT1 (AngII type 1) receptor antagonist], bosentan (ETA/ETB receptor antagonist) or losartan+bosentan. Pacing-induced rises in LAP (left atrial pressure) were amplified by the simultaneous administration of separate AngII and ET-1, and attenuated following blockade of the peptides, with maximum effects observed during combined treatments. Although these changes in atrial pressure were paralleled by concomitant alterations in circulating levels of both ANP (atrial natriuretic peptide) and BNP (brain natriuretic peptide), the plasma natriuretic peptide/atrial pressure relationship tended to be augmented by AngII and ET-1 and diminished by their blockade. A significant difference was demonstrated between the enhanced plasma BNP response to increasing LAP during combined AngII+ET-1 administration and decreased response during losartan+bosentan treatment (P<0.05). A similar, but non-significant, trend was evident for ANP. The present study indicates dual AngII/ET-1 blockade diminishes BNP (and to a lesser extent ANP) secretion in developing heart failure, suggesting that augmentation of the natriuretic peptide system during the combination of these therapies may be of benefit.
33
Goetze, Jens P. "B-Type Natriuretic Peptide: From Posttranslational Processing to Clinical Measurement." Clinical Chemistry 58, no. 1 (January 1, 2012): 83–91. http://dx.doi.org/10.1373/clinchem.2011.165696.
Full textAbstract:
Abstract BACKGROUND Plasma cardiac natriuretic peptides and peptide fragments from their molecular precursors are markers of heart disease. Clinical studies have defined the current diagnostic utility of these markers, whereas biochemical elucidation of peptide structure and posttranslational processing has revealed new plasma peptide forms of potential clinical use. CONTENT Natriuretic propeptide structures undergo variable degrees of endo- and exoproteolytic cleavages as well as amino acid modifications, which leave the plasma phase of the peptides highly heterogeneous and dependent on cardiac pathophysiology and capacity. An ongoing characterization of the molecular heterogeneity may not only help us to appreciate the biosynthetic capacity of the endocrine heart but may also lead to the discovery of new and more disease-specific targets for future molecular diagnosis. SUMMARY Peptides derived from pro–atrial natriuretic peptide and pro–B-type natriuretic peptide are useful plasma markers in heart failure. New data have defined cardiac myocytes as competent endocrine cells in posttranslational processing and cellular secretion.
34
Codognotto, Marta, Antonio Piccoli, Martina Zaninotto, Monica Mion, Mario Plebani, Ugo Vertolli, Francesco Tona, Luisa Ruzza, Agata Barchita, and Giovanni M. Boffa. "Renal Dysfunction Is a Confounder for Plasma Natriuretic Peptides in Detecting Heart Dysfunction in Uremic and Idiopathic Dilated Cardiomyopathies." Clinical Chemistry 53, no. 12 (December 1, 2007): 2097–104. http://dx.doi.org/10.1373/clinchem.2007.089656.
Full textAbstract:
Abstract Background: The diagnostic value of natriuretic peptides in uremic cardiomyopathy has not been defined, nor has the effect of a hemodialysis (HD) session on peptides. Methods: We performed an observational study of 100 white adult outpatients in New York Heart Association class I–II, with neither diabetes nor ischemic heart disease, 50 of whom had idiopathic dilated cardiomyopathy (DCM) and 50 of whom had uremic cardiomyopathy and were undergoing HD. We measured plasma N-terminal proB-type natriuretic peptide (NT-proBNP), BNP, and atrial natriuretic peptide (ANP) both before and after a dialysis session. Doppler echocardiograms were evaluated. We performed multiple regression analysis on the logarithm of peptide concentrations using clinical, laboratory, and echocardio-Doppler data as explanatory variables. Results: Mean peptide concentrations were higher in the HD group, with an HD:DCM ratio of 25 for NT-proBNP and 5 for BNP and ANP. Peptides were correlated with each other (r > 0.85). After HD, NT-proBNP significantly increased by 14%, BNP decreased by 17%, and ANP decreased by 56%. Predialysis concentrations correlated with postdialysis values (r > 0.85). A multiple regression equation significantly fitted the observed peptide concentrations, both pre- and postdialysis, using the same set of 4 variables: disease group (DCM or HD), diastolic pattern, left atrial volume, and body mass index. Conclusions: Renal dysfunction was a confounder for natriuretic peptides, which were present in higher concentrations in the uremic patients with milder cardiac dysfunction than in those with idiopathic DCM without renal dysfunction. Left diastolic function pattern and atrial volume were cardiac determinants of peptide concentrations in DCM and HD.
35
Kellner, Michael, Ines Diehl, Kristina Knaudt, Cornelius Schüle, Holger Jahn, and Klaus Wiedemann. "C-type natriuretic peptide exerts stimulatory effects on the corticotropin-releasing hormone-induced secretion of hormones in normal man." European Journal of Endocrinology 136, no. 4 (April 1997): 388–93. http://dx.doi.org/10.1530/eje.0.1360388.
Full textAbstract:
Abstract C-type natriuretic peptide and atrial natriuretic peptide have been reported to bind to distinct receptors and to exert opposing effects on different systems. Although it is known that atrial natriuretic peptide inhibits the corticotropin-releasing hormone-stimulated hormone release in man, the corresponding action of C-type natriuretic peptide has so far not been characterized. We investigated the effects of 30-min infusions of 150 and 300 μg C-type natriuretic peptide on adrenocorticotropin, cortisol, and prolactin release stimulated by 100 μg corticotropin-releasing hormone and on cardiovascular parameters in 8 healthy male volunteers. Compared with placebo, 300 μg C-type natriuretic peptide significantly (P<0·05) enhanced the stimulation of cortisol (area under curve (arbitrary units): 520 ± 35 vs 651 ± 55) and prolactin (area under curve: 29 ± 3 vs 37 ± 5). Adrenocorticotropin levels were increased, but the differences did not reach statistical significance (maximum increment: 27±4 vs 36± 2 pg/ml). C-type natriuretic peptide at a dose of 150 μg had no clear effect on these hormones and C-type natriuretic peptide also produced no cardiovascular or subjective effects. Our data suggest stimulatory effects of C-type natriuretic peptide on corticotropinreleasing hormone-induced hormone release and offer further evidence for a complex role of different natriuretic peptides in endocrine regulation. European Journal of Endocrinology 136 388–393
36
Lang, Chim C., Joseph G. Motwani, Wendy J. R. Coutie, and Allan D. Struthers. "Clearance of brain natriuretic peptide in patients with chronic heart failure: indirect evidence for a neutral endopeptidase mechanism but against an atrial natriuretic peptide clearance receptor mechanism." Clinical Science 82, no. 6 (June 1, 1992): 619–23. http://dx.doi.org/10.1042/cs0820619.
Full textAbstract:
1. Brain natriuretic peptide is a new natriuretic hormone with striking similarity to atrial natriuretic peptide, but there are no previous data concerning its clearance in man. Two pathways of clearance for atrial natriuretic peptide are recognized: degradation by neutral endopeptidase and binding to atrial natriuretic peptide clearance receptors. We have examined the effect of candoxatril, an inhibitor of neutral endopeptidase (dose range 10–200 mg), and the effect of an infusion of a pharmacological dose [45 μg (90 μg in two patients)] of synthetic human atrial natriuretic peptide on plasma human brain natriuretic peptide-like immunoreactivity levels in seven patients with mild to moderate chronic heart failure. 2. Plasma human brain natriuretic peptide-like immunoreactivity levels were elevated in all patients (mean ± sem 22.0 ± 6.2 pmol/l) compared with healthy control subjects (1.3 ± 0.2 pmol/l, n = 11). 3. In all patients, candoxatril increased both plasma atrial natriuretic peptide (P < 0.05) and plasma human brain natriuretic peptide-like immunoreactivity (P < 0.05) levels. 4. By contrast, an exogenous infusion of atrial natriuretic peptide had no effect on plasma human brain natriuretic peptide-like immunoreactivity levels despite increasing the plasma atrial natriuretic peptide concentration to 424 ± 74 pmol/l, which is a level of atrial natriuretic peptide which would have ‘swamped’ all atrial natriuretic peptide clearance receptors. 5. We have therefore shown that plasma human brain natriuretic peptide-like immunoreactivity levels in chronic heart failure are increased by a neutral endopeptidase inhibitor, but are unchanged by an exogenous infusion of atrial natriuretic peptide. Our results suggest that in patients with chronic heart failure, degradation by neutral endopeptidase is an important pathway for clearance of brain natriuretic peptide. By an indirect approach, we did not find any evidence of a role for atrial natriuretic peptide clearance receptors in the metabolism of brain natriuretic peptide in these patients. Although this is in agreement with work in vitro, there could be alternative explanations for the lack of a change in circulating human brain natriuretic peptide-like immunoreactivity during exogenous administration of atrial natriuretic peptide.
37
Vesely, David L. "Natriuretic peptides and acute renal failure." American Journal of Physiology-Renal Physiology 285, no. 2 (August 2003): F167—F177. http://dx.doi.org/10.1152/ajprenal.00259.2002.
Full textAbstract:
Atrial natriuretic peptides (ANPs) are a family of peptide hormones, e.g., ANP, long-acting natriuretic peptide, vessel dilator, and kaliuretic peptide synthesized by the ANP gene. Brain natriuretic peptide (BNP) and C-type natriuretic peptide are also members of this family but are synthesized by separate genes. Within the kidney, the ANP prohormone's posttranslational processing is different from that of other tissues, resulting in an additional four amino acids added to the NH2terminus of ANP (e.g., urodilatin). Each of these natriuretic and diuretic peptides increases within the circulation with acute renal failure (ARF). Renal transplantation but not hemodialysis returns their circulating concentrations to those of healthy individuals. BNP and adrenomedullin, a 52-amino acid natriuretic peptide, have beneficial effects on glomerular hypertrophy and glomerular injury but do not improve tubular injury (i.e., acute tubular necrosis). Vessel dilator ameliorates acute tubular necrosis with regeneration of the brush borders of proximal tubules. Vessel dilator decreases mortality in ARF from 88 to 14% at day 6 of ARF, even when given 2 days after renal failure has been established.
38
Cheung, B. M. Y., J. E. C. Dickerson, M. J. Ashby, M. J. Brown, and J. Brown. "Effects of Physiological Increments in Human α-Atrial Natriuretic Peptide and Human Brain Natriuretic Peptide in Normal Male Subjects." Clinical Science 86, no. 6 (June 1, 1994): 723–30. http://dx.doi.org/10.1042/cs0860723.
Full textAbstract:
1. Brain natriuretic peptide, closely related to atrial natriuretic peptide in structure, may be an important circulating hormone. Its physiological role is unclear. First, we studied the effects of incremental infusions of brain natriuretic peptide in six healthy men on plasma brain natriuretic peptide levels and the pharmacokinetics of brain natriuretic peptide. Synthetic human brain natriuretic peptide-32 was infused intravenously, at an initial rate of 0.4 pmol min−1 kg−1, doubling every 15 min until the dose rate reached 6.4 pmol min−1 kg−1, at which rate the infusion was maintained for 30 min. 2. The brain natriuretic peptide infusion raised the brain natriuretic peptide-like immunoreactivity from 1.4 ± 0.5 pmol/l to 21.4 ± 7.6 pmol/l. Brain natriuretic peptide-like immunoreactivity after the end of infusion was consistent with a bi-exponential decay, with half-lives of 2.1 min and 37 min. 3. Next, we studied the effects of low-dose infusion of brain natriuretic peptide to mimic physiological increments in the circulating levels in comparison with atrial natriuretic peptide. Six dehydrated male subjects received intravenous infusions of atrial natriuretic peptide and brain natriuretic peptide, separately and in combination, in a randomized double-blind, placebo-controlled, four-part cross-over design. Atrial natriuretic peptide and brain natriuretic peptide were given at the rate of 0.75 and 0.4 pmol min−1 kg−1, respectively, for 3 h. The control infusion consisted of the vehicle. 4. Analysis of variance showed that atrial natriuretic peptide and atrial natriuretic peptide plus brain natriuretic peptide, but not brain natriuretic peptide alone, increased urinary flow and decreased urinary osmolality significantly. However, urinary sodium excretion was significantly increased by atrial natriuretic peptide, brain natriuretic peptide and atrial natriuretic peptide plus brain natriuretic peptide. 5. None of the four infusates significantly altered the blood pressure, heart rate or glomerular filtration rate. 6. This study showed, for the first time, that physiological increments in brain natriuretic peptide, like those in atrial natriuretic peptide, are natriuretic. Although atrial natriuretic peptide and brain natriuretic peptide do not appear to interact synergistically, they are likely to act in concert in the physiological regulation of sodium balance.
39
Otani, Kentaro, Takeshi Tokudome, Chizuko A. Kamiya, Yuanjie Mao, Hirohito Nishimura, Takeshi Hasegawa, Yuji Arai, et al. "Deficiency of Cardiac Natriuretic Peptide Signaling Promotes Peripartum Cardiomyopathy-Like Remodeling in the Mouse Heart." Circulation 141, no. 7 (February 18, 2020): 571–88. http://dx.doi.org/10.1161/circulationaha.119.039761.
Full textAbstract:
Background: The maternal circulatory system and hormone balance both change dynamically during pregnancy, delivery, and the postpartum period. Although atrial natriuretic peptides and brain natriuretic peptides produced in the heart control circulatory homeostasis through their common receptor, NPR1, the physiologic and pathophysiologic roles of endogenous atrial natriuretic peptide/brain natriuretic peptide in the perinatal period are not fully understood. Methods: To clarify the physiologic and pathophysiologic roles of the endogenous atrial natriuretic peptide/brain natriuretic peptide–NPR1 system during the perinatal period, the phenotype of female wild-type and conventional or tissue-specific Npr1-knockout mice during the perinatal period was examined, especially focusing on maternal heart weight, blood pressure, and cardiac function. Results: In wild-type mice, lactation but not pregnancy induced reversible cardiac hypertrophy accompanied by increases in fetal cardiac gene mRNAs and ERK1/2 (extracellular signaling-regulated kinase) phosphorylation. Npr1-knockout mice exhibited significantly higher plasma aldosterone level than did wild-type mice, severe cardiac hypertrophy accompanied by fibrosis, and left ventricular dysfunction in the lactation period. Npr1-knockout mice showed a high mortality rate over consecutive pregnancy–lactation cycles. In the hearts of Npr1-knockout mice during or after the lactation period, an increase in interleukin-6 mRNA expression, phosphorylation of signal transducer and activator of transcription 3, and activation of the calcineurin–nuclear factor of the activated T cells pathway were observed. Pharmacologic inhibition of the mineralocorticoid receptor or neuron-specific deletion of the mineralocorticoid receptor gene significantly ameliorated cardiac hypertrophy in lactating Npr1-knockout mice. Anti–interleukin-6 receptor antibody administration tended to reduce cardiac hypertrophy in lactating Npr1-knockout mice. Conclusions: These results suggest that the characteristics of lactation-induced cardiac hypertrophy in wild-type mice are different from exercise-induced cardiac hypertrophy, and that the endogenous atrial natriuretic peptide/brain natriuretic peptide–NPR1 system plays an important role in protecting the maternal heart from interleukin-6–induced inflammation and remodeling in the lactation period, a condition mimicking peripartum cardiomyopathy.
40
Duggan, J., S. Kilfeather, S. L. Lightman, E. O'Brien, and K. O'Malley. "Plasma atrial natriuretic peptide concentration and platelet atrial natriuretic peptide binding site density in ageing and hypertension." Clinical Science 81, s25 (October 1, 1991): 509–14. http://dx.doi.org/10.1042/cs0810509.
Full textAbstract:
1. Ageing and hypertension are associated with changes in the way in which the body handles sodium. This may involve changes in plasma atrial natriuretic peptide concentration, since atrial natriuretic peptide is a regulator of sodium handling by the kidney and the plasma atrial natriuretic peptide concentration is increased in both ageing and hypertension. An increase in the plasma atrial natriuretic peptide concentration could also be associated with a change in atrial natriuretic peptide receptor density, possibly involving down-regulation. 2. To investigate these possibilities plasma atrial natriuretic peptide concentration and platelet atrial natriuretic peptide binding site density were measured in 18 young, 11 middle-aged and 12 elderly healthy subjects and in 23 patients with mild to moderate essential hypertension. 3. In normotensive subjects, the plasma atrial natriuretic peptide concentration increased with age (r = 0.49, P < 0.01) and was significantly higher in elderly than young subjects (mean ± sem, 31.9 ± 4.5 versus 18.3 ± 2.0 pmol/l, P < 0.05). The plasma atrial natriuretic peptide concentration increased with the mean arterial pressure in normotensive subjects (r = 0.47, P < 0.01). Multiple regression analysis did not show independent relationships between the plasma atrial natriuretic peptide concentration and either age or mean arterial pressure in normotensive subjects alone. However, when normotensive subjects and hypertensive patients were considered together, multiple regression revealed both age and mean arterial pressure as independent predictors of the plasma atrial natriuretic peptide concentration (P < 0.05, P < 0.01, respectively). In normotensive subjects, the platelet atrial natriuretic peptide binding site density did not change with age (r = 0.19, P = 0.27). 4. The plasma atrial natriuretic peptide concentration was elevated in hypertensive patients (37.6 ± 2.5 versus 30.4 ± 3.1 pmol/l, P < 0.05). There was no significant difference in the platelet atrial natriuretic peptide binding site density between hypertensive patients and normotensive subjects. 5. It is concluded that the plasma atrial natriuretic peptide concentration increases with age. The exact mechanism is uncertain, but it may play a role in the altered renal sodium handling seen with age. The elevation in the plasma atrial natriuretic peptide concentration with age is insufficient to induce a secondary reduction in atrial natriuretic peptide binding site density. Similarly, the elevation of the plasma atrial natriuretic peptide concentration in patients with mild to moderate hypertension does not lead to down-regulation of platelet atrial natriuretic peptide binding site density. It appears that increases in circulating atrial natriuretic peptide, greater than those observed in ageing and moderate hypertension, are required to induce down-regulation of platelet atrial natriuretic peptide binding site density.
41
Kenny, A. J., A. Bourne, and J. Ingram. "Hydrolysis of human and pig brain natriuretic peptides, urodilatin, C-type natriuretic peptide and some C-receptor ligands by endopeptidase-24.11." Biochemical Journal 291, no. 1 (April 1, 1993): 83–88. http://dx.doi.org/10.1042/bj2910083.
Full textAbstract:
Endopeptidase-24.11 (E-24.11, EC 3.4.24.11) is widely believed to play a physiological role in metabolizing atrial natriuretic peptide (ANP). Since the discovery of ANP, new natriuretic peptides have been isolated and other peptides synthesized as receptor ligands. The hydrolysis in vitro of six related peptides by the endopeptidase has been studied, mainly by h.p.l.c. The initial attack on the 32-residue form of pig brain natriuretic peptide (pBNP-32) was shown to be at the Ser20-Leu21 bond, as had been previously shown for the 26-residue form. In contrast, human brain natriuretic peptide-32 (hBNP-32), which differs in ten residues from pBNP-32, was attacked first at the Met4-Val5 bond, releasing the N-terminal tetrapeptide, and only later at bonds within the ring: at Arg17-Ile18 and subsequently at four other sites. Urodilatin, which has a four-residue extension at the N-terminus compared with alpha-human atrial natriuretic peptide-28 (alpha-hANP), was degraded at about half the rate of the latter, though the C-terminal Phe-Arg-Tyr was released at the same rate. The 22-residue C-type natriuretic peptide was hydrolysed more rapidly than alpha-hANP, as were two C-receptor ligands (peptides with deletions within the ring): C-ANP4-23 (rANP4-23 des-Gln18,Ser19,Gly20,Leu21,Gly22) and SC 46542 (hANP5-28 des-Phe8,Gly9,Ala17,Gln18). Angiotensin-converting enzyme failed to hydrolyse pBNP-32, hBNP-32 or 125I-rat (r) ANP, even after prolonged incubation. Km and kcat values were determined for the hydrolysis of alpha-hANP, porcine BNP-26, porcine BNP-32 and 125I-rANP by E-24.11. Ki values were determined for six peptides, alpha-hANP, urodilatin, hBNP-32, C-type natriuretic peptide (CNP), SC 46542 and C-type natriuretic peptide (C-ANP4-23), in radiometric assays of E-24.11 with either [125I] insulin B chain or [125I] rANP as substrate. The Ki values (2.5-13 microM) for CNP were the lowest of any of the group, whereas those for hBNP-32 (151-172 microM) were the highest. The physiological significance of these results is discussed, especially in regard to the relative resistance of hBNP-32 to attack and the ability of the C-receptor ligands to compete with natriuretic peptides for hydrolysis by E-24.11.
42
Cahill, P. A., and A. Hassid. "ANF-C-receptor-mediated inhibition of aortic smooth muscle cell proliferation and thymidine kinase activity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, no. 1 (January 1, 1994): R194—R203. http://dx.doi.org/10.1152/ajpregu.1994.266.1.r194.
Full textAbstract:
We have investigated the inhibition of DNA synthesis and cell proliferation by rat atrial natriuretic factor [rANF-(99-126)] and several synthetic peptides that bind selectively to the ANF-C-type clearance receptors in subcultured aortic smooth muscle cells. These peptides decreased serum-induced 1) [3H]thymidine incorporation, 2) cell proliferation, and 3) thymidine kinase activity without altering basal or elevated cAMP or cGMP levels. In contrast, another ANF-C-receptor-binding peptide, des[Gln116,Ser117,Gly118,Leu119,Gly120] rANF-(102-121)-NH2 (cANF), failed to decrease serum-induced mitogenesis, yet 100 nM cANF reversed the inhibition of DNA synthesis and cell proliferation and the decrease of thymidine kinase activity elicited by other C receptor-binding peptides, including rANF-(99-126), rANF-(103-125), and porcine C-type natriuretic peptide [pCNP-(1-22)]. Delayed addition experiments indicated that atrial peptides influence a relatively late event (or events) during the G1 phase of the cell cycle. The inhibition of DNA synthesis by C-receptor-binding atrial peptides appeared to be selective for aortic smooth muscle cells, inasmuch as a potent inhibitory agonist peptide, Cys116-rANF-(102-116), was without significant influence on the incorporation of thymidine in cultured rat mesangial cells or bovine pulmonary artery endothelial cells. These results indicate that atrial natriuretic peptide analogues decrease vascular smooth muscle cell mitogenesis and proliferation by a cyclic nucleotide-independent mechanism involving the C-type receptor. Moreover the inhibition of DNA synthesis by rANF-(99-126) and the neuropeptide pCNP-(1-22) appears to be mediated by the ANF-C-type receptor and is associated with inhibition of thymidine kinase activity.
43
Kishimoto, Ichiro, F. Kent Hamra, and David L. Garbers. "Apparent B-type natriuretic peptide selectivity in the kidney due to differential processing." Canadian Journal of Physiology and Pharmacology 79, no. 8 (August 1, 2001): 715–22. http://dx.doi.org/10.1139/y01-049.
Full textAbstract:
Two natriuretic peptides, atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP), are found principally in the heart. In preliminary experiments with mouse kidney cells or slices, we found mouse BNP1-45 much more potent than ANP1-28 in causing elevations of cGMP (>50-fold). The guanylyl cyclase-A (GC-A) receptor has been suggested to represent the primary means by which both peptides signal. In cultured cells overexpressing GC-A, BNP and ANP were almost equivalent in potency, suggesting that a receptor unique for BNP exists in the kidney. However, in mice lacking the GC-A gene, neither BNP nor ANP significantly elevated cGMP in kidney slices. Phosphoramidon, a neutral endopeptidase inhibitor, shifted the apparent potency of ANP to values equivalent to that of BNP, suggesting these kidney cell/slices rapidly degrade ANP but not BNP. Mass spectroscopic analysis confirmed that ANP is rapidly cleaved at the first cysteine of the disulfide ring, whereas BNP is particularly stable to such cleavage. Other tissues (heart, aorta) failed to significantly degrade ANP or BNP, and therefore the kidney-specific degradation of ANP provides a mechanism for preferential regulation of kidney function by BNP independent of peripheral ANP concentration.Key words: guanylyl cyclase-A, atrial natriuretic peptide, B-type natriuretic peptide, neutral endopeptidase.
44
Ichiki, Tomoko, Atsushi Jinno, and Yoshihisa Tsuji. "Natriuretic Peptide-Based Novel Therapeutics: Long Journeys of Drug Developments Optimized for Disease States." Biology 11, no. 6 (June 3, 2022): 859. http://dx.doi.org/10.3390/biology11060859.
Full textAbstract:
The field of natriuretic peptides (NPs) as an endocrine hormone has been developing since 1979. There are three peptides in humans: atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP), which bind to the guanylyl cyclase-A (GC-A) receptor (also called natriuretic peptide receptor-A (NPR-A)), and C-type natriuretic peptide (CNP), which binds to the GC-B receptor (also called the NPR-B) and then synthesizes intracellular cGMP. GC-A receptor stimulation has natriuretic, vasodilatory, cardiorenal protective and anti-renin–angiotensin–aldosterone system actions, and GC-B receptor stimulation can suppress myocardial fibrosis and can activate bone growth before epiphyseal plate closure. These physiological effects are useful as therapeutics for some disease states, such as heart failure, hypertension, and dwarfism. To optimize the therapeutics for each disease state, we must consider drug metabolism, delivery systems, and target receptor(s). We review the cardiac NP system; new designer NPs, such as modified/combined NPs and modified peptides that can bind to not only NP receptors but receptors for other systems; and oral drugs that enhance endogenous NP activity. Finally, we discuss prospective drug discoveries and the development of novel NP therapeutics.
45
Koepke, J. P., S. Jones, and G. F. DiBona. "Renal nerves mediate blunted natriuresis to atrial natriuretic peptide in cirrhotic rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 252, no. 5 (May 1, 1987): R1019—R1023. http://dx.doi.org/10.1152/ajpregu.1987.252.5.r1019.
Full textAbstract:
The diuretic and natriuretic responses to atrial natriuretic peptide in conscious rats with cirrhosis (chronic bile duct ligation) were examined. Cirrhotic rats had sodium retention, ascites, and elevated liver weights. In conscious control rats, atrial natriuretic peptide increased urine flow rate and urinary sodium excretion. In conscious cirrhotic rats, atrial natriuretic peptide had no effect on urine flow rate or urinary sodium excretion. Renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide in cirrhotic rats. Renal sympathetic nerve activity increased in conscious cirrhotic rats during infusion of atrial natriuretic peptide but decreased in conscious control rats. Inhibition of the renin-angiotensin system with captopril had no effect on the diuretic or natriuretic responses to atrial natriuretic peptide in conscious control or cirrhotic rats. Mean arterial pressure, glomerular filtration rate, and renal plasma flow were affected similarly by atrial natriuretic peptide in control and cirrhotic rats. Increased renal sympathetic nerve activity, but not angiotensin II, mediates the blunted diuretic and natriuretic responses to atrial natriuretic peptide in conscious cirrhotic rats.
46
Cargill, Robert I., Allan D. Struthers, and Brian J. Lipworth. "Comparative Effects of Atrial Natriuretic Peptide and Brain Natriuretic Peptide on the Aldosterone and Pressor Responses to Angiotensin Ii in Man." Clinical Science 88, no. 1 (January 1, 1995): 81–86. http://dx.doi.org/10.1042/cs0880081.
Full textAbstract:
1. Atrial natriuretic peptide and brain natriuretic peptide have similar vasodilator and natriuretic properties, although little information is available regarding their relative effects as antagonists of the renin—angiotensin—aldosterone system. We have therefore compared how atrial natriuretic peptide and brain natriuretic peptide affect the systemic pressor and aldosterone responses to angiotensin II in eight male subjects. 2. Each subject was studied on three separate occasions, when they received a 60-min infusion of placebo, atrial natriuretic peptide (10 pmol min−1 kg−1) or brain natriuretic peptide (10 pmolmin−1 kg−1), with a concomitant infusion of angiotensin II (6 ng min−1 kg−1) given for the final 30 min of the infusion period. The change in haemodynamic parameters and plasma aldosterone induced by angiotensin II was measured. Plasma concentrations of atrial natriuretic peptide (182 ± 23 pmol/l) and brain natriuretic peptide (193 ± 25 pmol/l) achieved at steady-state during the infusion on each study day were not significantly different. 3. Increases in mean arterial pressure in response to angiotensin II were significantly lowered by concomitant infusion of atrial natriuretic peptide (21.0 ± 1.7 mmHg) and brain natriuretic peptide (20.1 ± 1.9 mmHg) compared with placebo (29.0 ± 4.1 mmHg). There were similar effects on systolic and diastolic blood pressure. Cardiac output was decreased on each study day to the same extent by angiotensin II infusion. Total systemic vascular resistance showed a non-significant trend towards an attenuated response to angiotensin II when atrial natriuretic peptide or brain natriuretic peptide was infused concomitantly in comparison with placebo. 4. Plasma aldosterone increased by 326 ± 49 pmol/l when angiotensin II was infused with placebo. Both atrial natriuretic peptide and brain natriuretic peptide significantly blunted this response, although the increase with atrial natriuretic peptide (19 ± 35 pmol/l) was significantly lower than the increase with brain natriuretic peptide (133 ± 19 pmol/l). 5. Atrial natriuretic peptide and brain natriuretic peptide were therefore equally effective in blunting the systemic pressor response to angiotensin II. It was apparent, however, in view of similar plasma concentrations at steady state, that on a molar basis atrial natriuretic peptide was a more potent inhibitor of angiotensin II-induced aldosterone secretion than brain natriuretic peptide. These results suggest a dissociation between the haemodynamic and hormonal effects of atrial natriuretic peptide and brain natriuretic peptide in terms of antagonism of the renin—angiotensin—aldosterone system.
47
Kishimoto, I., K. Nakao, S. Suga, K. Hosoda, T. Yoshimasa, H. Itoh, and H. Imura. "Downregulation of C-receptor by natriuretic peptides via ANP-B receptor in vascular smooth muscle cells." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (October 1, 1993): H1373—H1379. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1373.
Full textAbstract:
The natriuretic peptide system comprises at least three ligands, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) and three receptors, the ANP-A receptor, the ANP-B receptor, and the clearance (C) receptor. In the present study, the regulation of natriuretic peptide receptors by their ligands was investigated in cultured rat vascular smooth muscle cells (SMC). The treatment of vascular SMC with ANP, BNP, or CNP decreased the C-receptor density significantly, and the rank order of potency for this downregulation was CNP > ANP > BNP. This rank order was the same as that for guanosine 3',5'-cyclic monophosphate (cGMP) production by ANP, BNP, or CNP in vascular SMC and also the same as that for the ligand selectivity of the ANP-B receptor rather than the C-receptor. The incubation of vascular SMC with 8-bromoguanosine 3',5'-cyclic monophosphate significantly decreased the C-receptor density and its mRNA expression. These results suggest that the down-regulation of the C-receptor by natriuretic peptides is induced not by the binding of natriuretic peptides to the C-receptor but by the activation of the ANP-B receptor-cGMP pathway.
48
Supaporn, Thanom, Paul W. Wennberg, Chi-Ming Wei, Masahiko Kinoshita, Yuzuru Matsuda, and John C. Burnett. "Role for the Endogenous Natriuretic Peptide System in the Control of Basal Coronary Vascular Tone in Dogs." Clinical Science 90, no. 5 (May 1, 1996): 357–62. http://dx.doi.org/10.1042/cs0900357.
Full textAbstract:
1. While the natriuretic peptides (atrial, brain and C-type) mediate potent endothelium-independent vasorelaxing actions in vitro, the role of the endogenous natriuretic peptide system in vascular regulation in vivo remains unclear. 2. HS-142-1 is a novel natriuretic peptide receptor antagonist derived from a fungus named Aureobasidium sp. which selectively blocks particulate guanylate cyclase-linked natriuretic peptide A and B receptors that bind atrial, brain and C-type natriuretic peptide, and thus attenuates the generation of cGMP. 3. To characterize the vascular actions of the endogenous natriuretic peptide system in the control of basal coronary and systemic haemodynamics, six normal male mongrel anaesthetized dogs were studied while a second group of five dogs served as a control. HS-142-1 was given as an intravenous bolus at 3 mg/kg and was studied over five 20 min periods. 4. No significant difference after HS-142-1 was observed in mean arterial pressure, heart rate, cardiac output, right atrial pressure, pulmonary capillary wedge pressure or systemic vascular resistance compared with control. In contrast, a significant increase in coronary vascular resistance and decrease in coronary blood flow were observed which were different from the baseline values and the responses of the control group. 5. These studies demonstrate that HS-142-1 produces vasoconstriction in the coronary circulation. We conclude that the endogenous natriuretic peptide system, which is of cardiac and endothelial cell origin, is an important regulator of basal coronary vascular tone.
49
De Plater, G. M., R. L. Martin, and P. J. Milburn. "The Natriuretic Peptide (Onp-39) From Platypus (Ornithorhynchus anatinus) Venom Promotes Mast Cell Histamine Release." Australian Mammalogy 20, no. 2 (1998): 301. http://dx.doi.org/10.1071/am98303.
Full textAbstract:
In this study we investigated the possibility that the C-type natriuretic peptide from platypus venom (ONP-39) contributes to the acute effects of envenomation, which include oedema, pain and erythema. These effects may result from the release of auto pharmacological mediators from mast cells. Using an in vitro assay we have demonstrated that both ONP-39 and the endogenous C-type natriuretic peptide (CNP-22) release histamine from rat peritoneal mast cells, an effect similar to the structurally homologous atrial natriuretic peptide (ANP) (Opgenorth et al., 1990, Peptides 11(5):1003-7). Two synthetic peptides, ONP-39(1-17) and ONP-39(18-39), corresponding to the N- and C- termini respectively, are equipotent, suggesting that ONP-39 and other natriuretic peptides do not act through conventional ANP receptors on mast cells. The ability of ONP-39 to promote histamine release suggests that it may contribute to the acute symptoms of envenomation.
50
Angus, Robert M., Jane E. Nally, Raymond McCall, Louise C. Young, John C. McGrath, and Neil C. Thomson. "Modulation of the Effect of Atrial Natriuretic Peptide in Human and Bovine Bronchi by Phosphoramidon." Clinical Science 86, no. 3 (March 1, 1994): 291–95. http://dx.doi.org/10.1042/cs0860291.
Full textAbstract:
1. We have previously shown that atrial natriuretic peptide causes bronchodilatation and reduces bronchial reactivity when administered intravenously or by inhalation to asthmatic patients. We wished to determine the direct effect of exogenously applied atrial natriuretic peptide on isolated airway and the role of proteases important in atrial natriuretic peptide degradation in other organ systems. 2. The ability of atrial natriuretic peptide (α-human atrial natriuretic peptide 28-amino acid) to relax precontracted tissues and to protect against methacholine-induced contraction was studied in human and bovine tissue. The role of neutral endopeptidase-24.11 and other proteases in regulating the effect of atrial natriuretic peptide on bronchial smooth muscle was also examined by studying the influence of phosphoramidon, a protease inhibitor, whose actions include the inhibition of neutral endopeptidase-24.11, and the protease inhibitors leupeptin, aprotinin and soybean trypsin inhibitor on the airway response to atrial natriuretic peptide. 3. In human and bovine tissue atrial natriuretic peptide (10−6 mol/l) caused a slight relaxation of methacholine-contracted tissue [mean (SEM) percentage inhibition of contraction of 13.2 (3.02)% and 9.41 (2.63)% respectively] and evoked a signficant rightward shift of the cumulative concentration–-response curve to methacholine [pD2 5.15 (0.23) and 4.85 (0.1) compared with control values of 6.14 (0.1) and 5.85 (0.16), respectively]. 4. Phosphoramidon potentiated atrial natriuretic peptide-induced relaxation of methacholine-induced tone and the ability of atrial natriuretic peptide to protect against methacholine-induced contraction. The combination of leupeptine, aprotinin and soybean trypsin inhibitor did not significantly alter the bronchial response to atrial natriuretic peptide in either human or bovine tissues. 5. We conclude that in human and bovine tissue, atrial natriuretic peptide confers protection against methacholine-induced contraction and can relax induced tone and that inhibition of phosphoramidon-sensitive protease increases these effects of atrial natriuretic peptide on airway smooth muscle.