Relevant bibliographies by topics / Peptide natriuretico atriale

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Academic literature on the topic 'Peptide natriuretico atriale'

Author: Grafiati
Published: 21 February 2023
Last updated: 9 March 2023

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Journal articles on the topic "Peptide natriuretico atriale"

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.

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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.
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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.

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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.
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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.

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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.
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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.

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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.
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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.

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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.
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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.

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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.
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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.

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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.
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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.

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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.
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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.

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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+.
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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.

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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.
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Dissertations / Theses on the topic "Peptide natriuretico atriale"

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DELLA, CORTE Vittoriano. "RENAL SALT WASTING: UNA SINDROME DA INAPPROPRIATA SECREZIONE DI URODILATINA? UNO STUDIO PILOTA." Doctoral thesis, Università degli Studi di Palermo, 2022. https://hdl.handle.net/10447/554922.

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La Renal Salt Wasting Syndrome (RSW) è una sindrome clinica con caratteristiche di laboratorio che si sovrappongono completamente alla sindrome da secrezione inappropriata di ADH (SIADH). La differenza fondamentale tra le due sindromi risiede nel volume extracellulare (ECV), ridotto nella RSW e normale o leggermente aumentato nella SIADH. Le difficoltà nella diagnosi differenziale di questa sindrome e nella comprensione del preciso meccanismo patogenetico hanno contribuito a mettere in discussione l'esistenza stessa di RSW. Considerando le caratteristiche della RSW, è stato studiato il possibile ruolo dei peptidi natriuretici per spiegare la sua patogenesi come ANP e BNP, con risultati insoddisfacenti. Tuttavia, nessuno studio ha ancora indagato il possibile ruolo dell'urodilatina, un peptide appartenente alla famiglia dei peptidi natriuretici, che sembra avere un ruolo cruciale nella regolazione della sodiemia e del sodio urinario anche più dell'ANP. Abbiamo eseguito uno studio osservazionale retrospettivo, i pazienti sono stati divisi in 3 gruppi: un gruppo di pazienti senza iponatriemia e due gruppi di pazienti con iponatriemia, uno costituito da pazienti con RSW e l'altro costituito da pazienti con iponatriemia da altre cause. I pazienti con RSW mostrano livelli medi di urodilatina significativamente più elevati rispetto a entrambi i pazienti con (mediana 5,46 vs 0,57 ng/mL, p=0,006) o senza iponatriemia (mediana 5,46 vs 0,27 ng/mL, p<0,001). Livelli medi più elevati statisticamente significativi di urodilatina sono stati osservati anche quando i pazienti con RSW sono stati confrontati con gli altri due gruppi di pazienti considerati insieme (5,46 vs 0,32 ng/mL, test MW p<0,001). Al contrario, i livelli di proANP non erano statisticamente differenti tra i 3 sottogruppi (test KS complessivo p=0,266) o tra pazienti con RSW e pazienti con/senza iponatriemia (4,9 vs 9,7 nM, test MW p=0,122). Le prestazioni diagnostiche dei livelli medi di urodilatina per la diagnosi di RSW sono state valutate mediante la curva ROC. L'area sotto la curva (AUC) era 0,94 (IC 95% 0,86-1,00). Il miglior cut-off per i livelli medi di urodilatina, secondo l'indice di Youden, era di 2,87 ng/mL. A questo cut-off sensibilità, specificità, valore predittivo positivo e valore predittivo negativo erano, rispettivamente, 1,00, 0,88, 0,60 e 1,00. In conclusione, questo studio pilota ha mostrato risultati interessanti per quanto riguarda il dosaggio di urodilatina urinaria in pazienti con RSW, con implicazioni potenzialmente chiarificatrici e di utilità pratica sia per quanto riguarda la patogenesi di questa sindrome, sia per quanto riguarda i suoi criteri diagnostici e quindi sulla gestione clinica dei pazienti. Ci auguriamo che ulteriori studi futuri possano continuare a fare luce su questo interessante argomento.
Renal Salt Wasting Syndrome (RSW) is a clinical syndrome with laboratory characteristics completely overlapping with the syndrome of inappropriate ADH secretion (SIADH). The fundamental difference between the two syndromes lies in the extracellular volume (ECV), reduced in RSW and normal or slightly increased in SIADH. The difficulties in the differential diagnosis of this syndrome and in understanding the precise pathogenetic mechanism have contributed some authors to question the very existence of RSW. Considering the characteristics of RSW, natriuretic peptides were investigated to explain its onset such as ANP and BNP, with unsatisfactory results. However, no studies have yet investigated the possible role of urodilatin, a peptide belonging to the natriuretic peptide family, which seems to have a crucial role in regulating blood sodium and urinary sodium even more than ANP. We performed a retrospective observational study, the patients were divided into 3 groups: a group of patients without hyponatremia and two groups of patients with hyponatremia, one consisting of patients with RSW and the other consisting of patients with hyponatremia from other causes. patients with RSW display significantly higher mean urodilatin levels than both patients with (median 5.46 vs 0.57 ng/mL, p=0.006) or without hyponatremia (median 5.46 vs 0.27 ng/mL, p<0.001). Statistically significant higher mean levels of urodilatin were also observed when patients with RSW were compared with the other two groups of patients considered together (5.46 vs 0.32 ng/mL, MW test p<0.001). Conversely, proANP levels were not statistically different among the 3 subgroups (overall KS test p=0.266) or between patients with RSW and patients with/without hyponatremia (4.9 vs 9.7 nM, MW test p=0.122). Diagnostics performances of mean urodilatin levels for RSW diagnosis were evaluated by ROC curve. Area under the curve (AUC) was 0.94 (95%CI 0.86-1.00). Best cut-off for mean urodilatin levels, according to Youden’s index, was 2.87 ng/mL. At this cut-off sensitivity, specificity, positive predictive value and negative predictive value were, respectively, 1.00, 0.88, 0.60 and 1.00. In conclusion, this pilot study has shown interesting results regarding the dosage of urinary urodilatin in patients with RSW, with potentially clarifying implications and of practical utility both regarding the pathogenesis of this syndrome and regarding its diagnostic criteria and therefore on the clinical management of patients. We hope that further future studies can continue to shed light on this interesting topic.
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DE, VITO PAOLO. "Relazione tra pH intracellulare e produzione di specie reattive dell’ossigeno nella risposta immune innata: ruolo dello scambiatore sodio/idrogeno e del peptide natriuretico atriale." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2004. http://hdl.handle.net/2108/208231.

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Le cellule fagocitiche; monociti, macrofagi e neutrofili, sono i maggiori componenti della immunità innata. Tali cellule rispondono a stimoli infiammatori e/o immunitari attraverso meccanismi di difesa che si esplicano tramite la fagocitosi, la produzione di citochine e la generazione di specie reattive dell’ossigeno (ROS). I meccanismi di difesa operati dai fagociti sono selettivamente influenzati dal pH intracellulare (pHi) che è in genere regolato da differenti trasportatori di membrana tra cui lo scambiatore sodio/idrogeno (NHE). L’NHE opera l’influsso di ioni sodio ed il contemporaneo efflusso di ioni idrogeno in accordo con i rispettivi gradienti di concentrazione. Le funzioni di NHE non sono ristrette alla regolazione del pHi: lo scambiatore esercita anche un importante ruolo in diverse funzioni biologiche tra cui la proliferazione e il differenziamento cellulare, l’apoptosi e la riorganizzazione citoscheletrica. Inoltre, in diversi tumori, il microambiente extracellulare è più acido di quello che caratterizza i tessuti normali, e in queste condizioni l’NHE rappresenta l’unico sistema in grado di assicurare l’omeostasi del pHi. A questo riguardo, nel modello di carcinoma epatico umano (HepG2), i livelli di mRNA di NHE come l’attività dello scambiatore sono 10 e 3 volte superiori rispetto a quanto riportato per i normali epatociti. Variazioni del pHi in risposta a differenti agonisti possono rappresentare dei segnali precoci capaci di contribuire alla regolazione dell’attività delle fosfolipasi; una famiglia di enzimi in grado di generare dei lipidi bioattivi tra cui il diacilglicerolo (DAG) e l’acido fosfatidico (PA). Il DAG e il PA possono attivare l’enzima NADPH ossidasi, che rappresenta una importante sorgente di ROS nei fagociti. La NADPH ossidasi svolge un importante ruolo anche in altri sistemi cellulari tra cui le HepG2, dove la sua attivazione appare essere positivamente correlata all’inibizione della proliferazione cellulare. I monociti ed i macrogafi in risposta a degli stimoli infiammatori sono in grado di rilasciare il peptide natriuretico atriale (ANP), un piccolo ormone principalmente sintetizzato dai cardiomiociti atriali capace di promuovere la natriuresi, la diuresi e di contribuire alla regolazione della pressione sanguigna. L’ANP può anche regolare alcune funzioni immunitarie in quanto capace di contrastare l’espressione di alcuni mediatori infiammatori tra cui la ciclossigenasi-2 (COX2), l’ossido nitrico (NO) e il fattore di necrosi tumorale (TNF)-α.Sulla base dell’importante ruolo del pHi e della possibile relazione tra NHE e produzione di ROS, il presente studio è stato incentrato nel valutare l’effetto dell’ANP sul pHi, sull’attività di alcune fosfolipasi (Ce D) e sulla produzione di ROS nei monociti/macrofagi umani e nelle cellule HepG2. I risultati ottenuti hanno evidenziato un significativo decremento del pHi dovuto all’inibizione di NHE dopo stimolazione con ANP nei macrofagi e nelle cellule HepG2. Sia i monociti che i macrofagi si siano rivelati in grado di esprimere l’intero set dei recettori per i peptidi natriuretici (NPR-A,NPR-B e NPR-C), ma nessuna significativa variazione del pHi è stata evidenziata nei monociti stimolati con ANP. Tuttavia, il trattamento dei monociti con 5-(etil-N-isopropil)amiloride, uno specifico inibitore di NHE è stato in grado di riprodurre il modello di acidificazione osservato nei macrofagi dopo stimolazione con ANP. Nei macrofagi il decremento ANP-dipendente del pHi è apparso parallelo ad un incremento dell’attività della PLD e della PLC, mentre nelle cellule HepG2 l’acidificazione intracellulare è stata correlata unicamente dell’attivazione della PLD. Il decremento ANP-dipendente del pHi, è stato correlato alla produzione di messaggeri lipidici bioattivi quali il DAG e il PA che si sono dimostrati responsabili dell’attivazione della NADPH ossidasi sia nei macrofagi che nelle cellule HepG2. Infine, tutti gli effetti mediati dall’ANP sono stati riprodotti utilizzando un analogo troncato dell’ormone denominato cANF specifico per i recettori NPR-C.
Phagocytes, namely monocytes, macrophages, and neutrophils, are major components of innate immunity. They respond to inflammatory/immune insults by up-regulating their host defense functions, including phagocytosis, cytokine production, and generation of reactive oxygen species (ROS). The host defense functions of phagocytes are selectively influenced by intracellular pH (pHi) that is controlled by which several plasmamembrane acid-base transporters, including the Na+/H+ exchanger (NHE) which operate the exchange of extracellular Na+ with cytoplasmic H+ ions according to the concentration gradient. The functions of NHE are not only restricted to pHi homeostasis: the exchenger plays also an important role a variety of downstream events, including cell proliferation, cell differentiation, apoptosis, and cytoskeletal organization. Moreover, in several tumors, the extracellular microenviroment is more acidic with respect to normal tissues and, in these conditions, the NHE represents the only system able to regulate pHi homeostasis. In this contest, it was reported , in hepatocellular carcinoma (HepG2 cells), that NHE mRNA levels as well as the exchanger activity are respectively 10-and-3 fold higher than in normal hepatocytes, Changes in pHi in response to a variety of ligands may represent a signalling event for the regulation of phospholipase activities: a family of enzymes able to generate bioactive lipids such as diacyglycerol (DAG) and phosphatidic acid (PA). DAG as well as PA can activate the enzyme NADPHoxidase, an important source of ROS in phagocytes. The NADPHoxidase plays an important role also in other cell systems including HepG2, where its activation appears positively coupled to the inhibition cell proliferation. It is well known that monocytes and macrophages in response to inflammatory insults can release the atrial natriuretic peptide (ANP), an hormone mainly secreted by the heart atria able to induce natriuresis, vasodilation and contribute to the regulation of blood pressure. The ANP can also regulate several immune functions since its able to reduce production of proinflammatory mediators by inhibition of nitric oxide (NO), and cyclooxygenase-2 (COX2) as well as tumor necrosis factor (TNF)-α synthesis. On the basis of both the important role of pHi and the possible relationship between NHE and ROS generation, the present study was aimed to evaluate the effects of atrial natriuretic peptide (ANP) on intracellular pH (pHi), phospholipase (C and D) activities and (ROS) production in human monocytes, macrophages and HepG2 cells. A significant pHi decrease due to the NHE inhibition was observed in ANP-stimulated macrophages as well as in HepG2 cells. Conversely, even if both monocytes and macrophages were show to express all three natriuretic peptide receptors (NPR-A, NPR-B, and NPR-C), no significant effect on pHi was observed in monocytes stimulated with ANP. Nevertheless, the treatment of monocytes with 5-(N-ethyl-N-isopropyl)amiloride, a specific inhibitor of NHE was able to determine a decrease of pHi which was similar to the one observed in macrophages after ANP stimulation. In human macrophages the ANP-induced pHi decrease was paralleled by an increased activity of both phospholipase D (PLD) and phospholipase C (PLC), whereas in HepG2 cells the intracellular acidification was correlated only to an increased PLD activity. Our results suggest that second lipid messengers produced after ANP-induced pHi decrease, such DAG and PA, were able to promote the NADPH oxidase activation in human macrophages as well as in HepG2 cells. Finally, all ANP-effects were mediated by NPR-C receptors.
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Thompson, Justine Sarah. "Atrial natriuretic peptide and the pulmonary circulation." Thesis, University of Sheffield, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364381.

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Zhang, Jin. "Inhibition of pulsatile luteinizing hormone release by atrial natriuretic peptide and brain natriuretic peptide in the ovariectomized rat." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/29412.

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Atrial natriuretic peptide (ANP) of atrial myocyte origin, has been shown to play a role in the diuresis, natriuresis, and antagonism of angiotensin and vasopressin. However, it is now apparent that in addition to the production of the peptide in the heart and in its role in fluid and electrolyte homeostasis, it is also produced in the central nervous system participating in the regulation of pituitary hormone secretion. Administration of ANP through both central and peripheral routes has been shown to inhibit secretion of luteinizing hormone (LH) in the gonadectomized rat model. A better understanding of the modulatory role of ANP on LH secretion and its possible mechanisms will add to our knowledge of the effects of neuropeptides on reproductive function. Brain natriuretic peptide (BNP) is a bioactive peptide of 26 amino acid residues recently identified in porcine brain. The peptide exerts potent diuretic-natriuretic and vasorelaxant effects, in a manner similar to that of ANP. BNP has a remarkable high sequence homology to ANP, especially in the 17 amino acid ring formed by an intramolecular disulfide linkage which is required for biological activity. The presence of BNP with ANP in the mammalian brain and remarkable resemblance in their molecular structures and physiological functions implies that BNP may also exert an inhibitory effect on LH secretion like ANP. This research focused on the effects of centrally administered ANP and BNP on pulsatile LH secretion and their possible mechanisms of action in ovariectomized rats. After third ventricle infusion of ANP or BNP, inhibition of mean plasma LH level, LH pulse amplitude and pulse frequency was observed. In searching for the possible mechanisms of inhibitory effect of ANP or BNP on pulsatile LH secretion, the effect of inhibiting the endogenous opiate system with naloxone on the action of centrally administered ANP or BNP was tested. Application of naloxone reversed the inhibitory effect of ANP and BNP on mean plasma LH level and LH pulse amplitude, but in terms of pulse frequency, naloxone treatment failed to reverse the inhibitory effect of ANP or BNP. In separate experiments, pretreatment with pimozide, a dopaminergic receptor blocker, prevented the inhibitory action of ANP and BNP on LH secretion. After infusion of ANP or BNP, there were no significant decrease in mean plasma LH level, pulse amplitude and pulse frequency in the pimozide-pretreated rats. In summary, the present study shows that both ANP and BNP inhibit pulsatile LH secretion, suggesting that the inhibitory effects on LH secretion once thought to be mediated by ANP alone may be regulated through a dual mechanism involving both ANP and BNP. Furthermore, the inhibitory mechanisms may involve the interactions of ANP and BNP with central opiate system and dopaminergic system on LH secretion.
Medicine, Faculty of
Obstetrics and Gynaecology, Department of
Graduate
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Kao, Jonathan. "Atrial natriuretic peptide in aging rats : evidence for altered processing, secretion and receptor binding." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/28993.

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The recently discovered atrial natriuretic peptide (ANP) has potent diuretic, natriuretic and hypotensive effects, and is believed to be involved in the maintenance of sodium homeostasis in both normal and pathological conditions. The mammalian aging process is associated with a host of abnormalities that include, among others, a compromised ability to regulate sodium homeostasis. There are reports that demonstrate a positive correlation between plasma ANP levels and age in man; accordingly, the aim of this study was to examine whether age-related sodium imbalance is associated with disturbances in the homeostasis of ANP. Specifically, the intracellular storage, processing and secretion of ANP from the atrium was studied and associated with circulating ANP concentrations and ANP receptor binding kinetics. Studies were conducted with four groups of male Wistar rats designated as 1-, 3-, 10-, and 20-month-old. 24-hour renal clearances were conducted to assess age-related changes in renal functions. GFR and UNaV increased steadily from 1 to 10 months of age and decreased in the 20-month-old, while fractional excretion of water (FEH₂O) and sodium (FENa) declined initially (from 1 to 10 months) and then rose in the 20-month-old group. Circulating ANP levels in the rats was significantly correlated with the increase in age (N = 147, r = 0.59, p < 0.0005). Atria of the animals were isolated and superfused with a modified Langendorff apparatus. The spontaneous release of ANP increased from 1 to 3 months, and steadily decreased after 3 months. The results indicate that ANP secretion increases with maturation and thereafter declines with advancing age. ANP concentrations in the right and left atria were also quantified. The results revealed that atrial ANP content increased from 1 to 3 months and decreased progressively with age. There was a positive correlation between the rate of ANP release and atrial ANP content (N= 42, r=0.50, p<0.01), suggesting that the release of ANP from the right atrium was associated with the atrial content. The concurrence of a reduction in ANP secretion but with elevation in plasma ANP concentration in the aged (20-month-old) rats, suggests that there may be an impairment in renal clearance of ANP. It was established that the main molecular species present in the atrium was γ-ANP and that this was unaffected by age as assessed by reverse-phase high performance liquid chromatography (RP-HPLC) coupled with radioimmunoassay. The molecular forms of ANP secreted by the atrium consisted of predominantly α-ANP, with a smaller amounts of γ-ANP. γ-ANP constituted only 1% of the total secreted ANP in the 1-, 3-, or 10-month-old rats, but up to 8% was detected in 20-month-old rats. Although both α-ANP and γ-ANP were present in the circulation, the ratio of γ-ANP/α-ANP increased significantly with age. The concentration of γ-ANP in the plasma of the 20-month-old rats was two- to three-fold higher than in the two younger groups (1- and 3-month-old). These data imply that the post-transcriptional processing of prohormone γ-ANP to active α-ANP is altered with age. Radio-ligand binding experiments were carried out using glomerular ANP receptors to determine whether the age-related alterations in plasma ANP levels has an effect on the binding of ANP to its target tissues. Both the receptor density (Bmax) and the equilibrium dissociation constant (kd increased from 1 to 3 months but decreased from 3 to 20 months. Collectively, these results suggest that: 1) Aging affects atrial ANP content and consequently influences the release of ANP from the isolated atria. 2) The processing of prohormone γ-ANP to active α-ANP is modified with age. 3) Plasma levels of ANP increase with age, which may result in down-regulation of ANP receptor density and increased efficacy in receptor binding affinity. These may represent the compensatory responses.
Medicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
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6

Hetmanski, David John. "A study of atrial natriuretic peptide in pregnancy." Thesis, University of Nottingham, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335300.

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Peters, Christian G. "SNARE-Mediated Exocytosis of Atrial Natriuretic Peptide from Atrial Cardiac Myocytes." University of Toledo Health Science Campus / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=mco1179405759.

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Willeit, Peter. "Natriuretic peptides and cardiovascular disease." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648533.

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Taskinen, P. (Panu). "Mapping the cellular mechanisms regulating atrial natriuretic peptide secretion." Doctoral thesis, Oulun yliopisto, 1999. http://urn.fi/urn:isbn:9514252721.

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Abstract Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are cardiac hormones, which are involved in the regulation of blood pressure and fluid homeostasis. The major determinant for ANP and BNP release are atrial and ventricular wall stretch, but also some vasoactive factors such as endothelin-1 (ET-1) can enhance cardiac hormone secretion. The mechanical stretch rapidly activates multiple signal transduction pathways in cardiac cells, but the cellular mechanisms mediating stretch-induced ANP secretion are still unknown. The aim of the present study was to examine the cellular mechanisms of autocrine/paracrine factors and stretch-induced ANP secretion. Genistein, a potent protein tyrosine kinase (PTK) inhibitor, rapidly increased cardiac contractile force and ANP secretion in perfused rat heart. This effect of genistein may be unrelated to the inhibition of PTKs since this stimulation was blocked by a L-type calcium channel antagonist and Ca2+/calmodulin-dependent protein kinase II inhibitor. Pregnancy hormone relaxin increased heart rate and ANP secretion in perfused spontaneously beating heart, suggesting that relaxin may have a role in modulating cardiac function. Cellular mechanisms of atrial wall stretch-induced ANP secretion were also studied. This enhanced secretion was blocked by sarcoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin and PTK inhibitor lavendustin A, indicating that thapsigargin sensitive Ca2+ pools and activation of PTK orPTK cascade have an important role in the regulation of stretch-secretion coupling. In addition, protein phosphatase inhibitor okadaic acid accelerated stretch-induced ANP secretion, suggesting that precise balance of protein kinase and phosphatase activity plays a role in mechanical stretch-induced ANP secretion. Finally interactions of endothelial factors regulating ANP exocytosis were studied. The potent nitric oxide synthase inhibitor L-NAME increased basal and atrial wall stretch-induced ANP secretion in the presence of ET-1, suggesting that nitric oxide may tonically inhibit ANP secretion.
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Vaillancourt, Patrice A. "Modulation of atrial natriuretic peptide receptors in rat pregnancy." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0006/MQ44307.pdf.

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Books on the topic "Peptide natriuretico atriale"

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1947-, Samson Willis Kendrick, and Quirion Remi 1955-, eds. Atrial natriuretic peptides. Boca Raton, Fla: CRC Press, 1990.

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1937-, Brenner Barry M., and Laragh John H. 1924-, eds. Biologically active atrial peptides. New York, NY: Raven Press, 1987.

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1937-, Brenner Barry M., and Laragh John H. 1924-, eds. Advances in atrial peptide research. New York: Raven Press, 1988.

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Atrial natriuretic hormones. Englewood Cliffs, NJ: Prentice Hall, 1992.

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D, Struthers Allan, ed. Atrial natriuretic factor. Oxford: Blackwell Scientific, 1990.

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D, Struthers Allan, ed. Atrial natriuretic factor. Oxford: Blackwell Scientific, 1990.

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J, Mulrow Patrick, and Schrier Robert W, eds. Atrial hormones and other natriureticfactors. Bethesda, Md: American Physiological Society, 1987.

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1947-, Samson Willis Kendrick, and Levin Ellis R, eds. Natriuretic peptides in health and disease. Totowa, N.J: Humana Press, 1997.

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1939-, Needleman Philip, and UCLA Symposium on the Biological and Molecular Aspects of Atrial Factors (1988 : Steamboat Springs, Colo.), eds. Biological and molecular aspects of atrial factors: Proceedings of a director's sponsors-UCLA symposium held at Steamboat Springs, Colorado, January 17-23, 1988. New York: Liss, 1988.

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Speake, Paul Frederick. In vitro stimulation of atrial natriuretic peptide secretion from Guinea Pig atria. Manchester: University of Manchester, 1994.

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Book chapters on the topic "Peptide natriuretico atriale"

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Huang, Kui, Le Zhang, and Cuntai Zhang. "Atrial Natriuretic Peptide." In Encyclopedia of Gerontology and Population Aging, 1–8. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-69892-2_1064-1.

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Huang, Kui, Le Zhang, and Cuntai Zhang. "Atrial Natriuretic Peptide." In Encyclopedia of Gerontology and Population Aging, 544–51. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-22009-9_1064.

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Thomson, Neil C. "Atrial Natriuretic Peptides." In Airways Smooth Muscle: Peptide Receptors, Ion Channels and Signal Transduction, 115–29. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7362-8_5.

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Champion, Howard R., Nova L. Panebianco, Jan J. De Waele, Lewis J. Kaplan, Manu L. N. G. Malbrain, Annie L. Slaughter, Walter L. Biffl, et al. "Atrial Natriuretic Peptide (ANP)." In Encyclopedia of Intensive Care Medicine, 280. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1180.

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Machraoui, A., J. Gude, B. E. Braun, D. Jäger, B. Lemke, M. Krieg, and J. Barmeyer. "Atrial Natriuretic Peptide and Atrial Size." In Endocrinology of the Heart, 200–201. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83858-3_36.

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Quirion, Rémi. "Atrial Natriuretic Factors." In Neural and Endocrine Peptides and Receptors, 299–312. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5152-8_20.

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Weidmann, P., H. Saxenhofer, C. Ferrier, and S. G. Shaw. "Atrial natriuretic peptide in man." In Functional Morphology of the Endocrine Heart, 161–85. Heidelberg: Steinkopff, 1989. http://dx.doi.org/10.1007/978-3-642-72432-9_17.

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Lang, R. E., H. Ruskoaho, M. Toth, D. Ganten, T. Unger, and R. Dietz. "Mechanisms Controlling Release of Atrial Natriuretic Peptide." In Atrial Hormones and Other Natriuretic Factors, 19–31. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4614-7529-3_3.

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Meyer, Markus, and Wolf-Georg Forssmann. "Renal Actions of Atrial Natriuretic Peptide." In Natriuretic Peptides in Health and Disease, 147–70. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3960-4_9.

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Nutt, Ruth F., Terry M. Ciccarone, Stephen F. Brady, C. Dylion Colton, William J. Paleveda, Terry A. Lyle, Theresa M. Williams, Daniel F. Veber, Audrey Wallace, and Raymond J. Winquist. "Structure-activity studies of atrial natriuretic factor." In Peptides, 444–46. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-010-9595-2_130.

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Conference papers on the topic "Peptide natriuretico atriale"

1

Xing, J., P. Fu, KG Birukov, and AA Birukova. "Atrial Natriuretic Peptide Attenuates LPS-Induced Lung Vascular Leak." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5552.

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Tanable, A., Y. Yatomi, T. Ohashi, H. Oka, T. Kariya, and S. Kume. "EFFECTS OF HUMAN ATRIAL NATRIURETIC PEPTIDES ON SECRETION REACTION IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644873.

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Human atrial natriuretic peptide (h-ANP) has vasodilating and natriuretic properties, and inhibits smooth muscle contraction, renal renin secretion and adrenal aldosterone release. Although Schiffrin has reported that human platelets have receptors for ANP, its effects in platelets are not established in vivo. We therefore investigated the influence of h-ANP on secretion reaction in human platelets. Eight healthy subjects, males, aged 20 to 24 years, donated blood for the study. Citrated platelet-rich plasma (PRP) was incubated with or without h-ANP at 37 C for 2.5 minutes. The samples of 0.5 ml PRP then used to measure ADP induced aggregation, ATP release reaction and C-serotonin release reaction. H-ANP, at concentration of 1x10 -6M, decreased ADP induced aggregation (after h-ANP: 77.4±9.7 % of control aggregation), and inhibited ATP release reaction (after h-ANP: 31.8±13.1%). Serotonin releasereaction induced by ADP was also inhibited ( control: 15.3±2.2%, after h-ANP: 8.3±0.5 %). The inhibitory effect of h-ANP on aggregation and secretion reaction was maximal by 3 minutes. These data suggest that h-ANP inhibits secretion reaction in human platelets.
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Loureiro, H., J. Sellares, M. Ferrer, C. Esquinas, R. Piner, S. Ebmeyer, S. Giersdoff, and A. Torres. "Increase in Levels of Pro-Atrial Natriuretic Peptide during Weaning Failure." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3797.

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Kaczmarczyk, M., C. Otte, K. Wiedemann, L. Kuehl, K. Schultebraucks, C. Spitzer, and K. Wingenfeld. "Major depression and atrial natriuretic peptide: The role of adverse childhood experiences." In Abstracts of the 1st Symposium of the Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP) and Deutsche Gesellschaft für Biologische Psychiatrie (DGBP). Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1679180.

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Abston, Eric D., Nicole Sborz, Robert Weiss, Hunter Champion, and Clarke G. Tankersley. "Atrial Natriuretic Peptide Receptor (NPR-1) Deficiency Alters Cardiac Response To Ozone (O3)." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1725.

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Vazquez, Z., G. Cagle, A. Chu, P. Gordon, P. Haines, C. Mullin, J. Klinger, R. Karo, A. Palmisciano, and C. Ventetuolo. "The Effects of Left Atrial Appendage Closure on Natriuretic Peptide Levels and Cardiac Filling Pressures." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2049.

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Klinger, JR, H. Duong, J. Newton, and EO Harrington. "Atrial Natriuretic Peptide Inhibits Thrombin-Induced Pulmonary Endothelial Barrier Dysfunction Via a Non PKG Dependent Pathway." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2330.

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Natarajan, Ramesh, Harm J. Bogaard, Donatas Kraskauskas, and Norbert F. Voelkel. "Multi-Stage Modulation Of Atrial Natriuretic Peptide Determines Right Ventricular Failure In Experimentally-Induced Pulmonary Hypertension." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4889.

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Neumann, Roland, Roland Gerull, Mathias Nelle, Sven Schulzke, and Sven Wellmann. "Plasma pro-endothelin-1 and pro-atrial natriuretic peptide are associated with bronchopulmonary dysplasia in very preterm infants." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa244.

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10

Bugrova, Marina. "Post-embedding immunogold labeling of tissue sections in the study of the atrial natriuretic peptide in the experimental congestive heart failure." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.671.

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