Journal articles: 'Resine angiotensine'

1

Meng, Q. C., J. Durand, Y. F. Chen, and S. Oparil. "Effects of dietary salt on angiotensin peptides in kidney." Journal of the American Society of Nephrology 6, no. 4 (October 1995): 1209–15. http://dx.doi.org/10.1681/asn.v641209.

Full text

Abstract:

This study used a novel simple method for the extraction, separation, identification, and quantitation of angiotensin-like immunoactivity from tissue to examine the effects of altering dietary NaCl intake on intrarenal angiotensin I, II, and III levels in salt-sensitive, spontaneously hypertensive rats, salt-resistant Wistar-Kyoto rats, and Sprague-Dawley rats. Seven-week-old male spontaneously hypertensive rats, Wistar-Kyoto rats, and Sprague-Dawley rats were assigned randomly to a diet containing either 8% (high) or 1% (basal) salt and were maintained on these diets for 3 wk. Rats were then decapitated without prior anesthesia, and kidneys were rapidly (< 30 s) removed, snap frozen in liquid nitrogen, and stored at -80 degrees C. Frozen tissue was extracted in 2 M acetic acid and then subjected to solid-phase extraction with the cation exchange resin AG 50W X4. Angiotensin peptides were separated by reversed-phase high-performance liquid chromatography on a phenyl silica gel column with an eluent consisting of 20% acetonitrile in 0.1 M ammonium phosphate buffer, pH 4.9, and quantitated by radioimmunoassay. The elution of standard peptides under isocratic conditions revealed clear resolution of angiotensin I, II, and III and the (1-7) and (3-8) peptides. Recoveries of both labeled and unlabeled angiotensin peptide standards from the extraction step were > 90%. Renal angiotensin II stores were significantly higher in spontaneously hypertensive rats than in Wistar-Kyoto or Sprague-Dawley rats, independent of diet. Renal angiotensin II and III were further suppressed during dietary salt supplementation in both salt-resistant strains but not in the spontaneously hypertensive rat. These findings are consistent with an enhanced (compared with Wistar-Kyoto and Sprague-Dawley rats) role for angiotensin II in the kidney of the salt-sensitive, spontaneously hypertensive rat, particularly under conditions of dietary salt supplementation.

APA, Harvard, Vancouver, ISO, and other styles

2

Zangrillo, Alberto, Sergio Colombo, Anna Mara Scandroglio, Evgeny Fominskiy, Marina Pieri, Maria Grazia Calabrò, Paolo Federico Beccaria, et al. "Angiotensin II infusion and markers of organ function in invasively ventilated COVID-19 patients." Critical Care and Resuscitation 23, no. 2 (June 7, 2021): 215–24. http://dx.doi.org/10.51893/2021.2.oa9.

Full text

Abstract:

OBJECTIVE: The use of angiotensin II in invasively ventilated patients with coronavirus disease 2019 (COVID-19) is controversial. Its effect on organ function is unknown. DESIGN: Prospective observational study. SETTING: Intensive care unit (ICU) of a tertiary academic hospital in Milan, Italy. PARTICIPANTS: Adult patients receiving mechanical ventilation due to COVID-19. INTERVENTIONS: Use angiotensin II either as rescue vasopressor agent or as low dose vasopressor support. MAIN OUTCOME MEASURES: Patients treated before angiotensin II was available or treated in an adjacent COVID-19 ICU served as controls. For data analysis, we applied Bayesian modelling as appropriate. We assessed the effects of angiotensin II on organ function. RESULTS: We compared 46 patients receiving angiotensin II therapy with 53 controls. Compared with controls, angiotensin II increased the mean arterial pressure (median difference, 9.05 mmHg; 95% CI, 1.87–16.22; P = 0.013) and the Pao2/Fio2 ratio (median difference, 23.17; 95% CI, 3.46–42.88; P = 0.021), and decreased the odds ratio (OR) of liver dysfunction (OR, 0.32; 95% CI, 0.09–0.94). However, angiotensin II had no effect on lactate, urinary output, serum creatinine, C-reactive protein, platelet count, or thromboembolic complications. In patients with abnormal baseline serum creatinine, Bayesian modelling showed that angiotensin II carried a 95.7% probability of reducing the use of renal replacement therapy (RRT). CONCLUSIONS: In ventilated patients with COVID-19, angiotensin II therapy increased blood pressure and Pao2/Fio2 ratios, decreased the OR of liver dysfunction, and appeared to decrease the risk of RRT use in patients with abnormal baseline serum creatinine. However, all of these findings are hypothesis-generating only. TRIAL REGISTRATION: ClinicalTrials.gov NCT04318366.

APA, Harvard, Vancouver, ISO, and other styles

3

Selvam, R., K. C. Rohini, C. Arunan, and K. P. Subashchandran. "Synthesis of Biologically Important Angiotensin-II and Angiotensin-IV Peptides by Using 4-(2',4'-Dimethoxypenyl-Fmoc-Aminomethyl)phenoxy Resin." Asian Journal of Chemistry 25, no. 15 (2013): 8673–76. http://dx.doi.org/10.14233/ajchem.2013.14998.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Raff, H., and B. Jankowski. "Inhibition of aldosterone release by hypoxia in vitro: interaction with carbon monoxide." Journal of Applied Physiology 76, no. 2 (February 1, 1994): 689–93. http://dx.doi.org/10.1152/jappl.1994.76.2.689.

Full text

Abstract:

We have demonstrated that the aldosteronogenic pathway of the zona glomerulosa is unusually sensitive to modest changes in PO2 (Michaelis constant for O2 approximately 95 Torr). The current study evaluated the interaction of CO (the classic ligand for P-450 enzymes) and the decreases in O2 on aldosteronogenesis in vitro. Bovine adrenocortical zona glomerulosa cells were incubated for 2 h and stimulated with either adenosine 3′,5′-cyclic monophosphate (cAMP) or angiotensin II. Ten and 20% CO led to significant decreases in cAMP- and angiotensin II-stimulated aldosteronogenesis. The combination of 20% CO and moderate decreases in PO2 (from approximately 140 to approximately 100 Torr) led to an interactive decrease in aldosterone production. The conversion of corticosterone to aldosterone catalyzed by aldosterone synthase, which is the site of O2 sensitivity, was not significantly inhibited by CO. We conclude that the aldosterone pathway is not exceptionally sensitive to CO compared with other steroidogenic pathways. This observation suggests that the unique O2-sensitive properties of the aldosterone pathway located primarily within aldosterone synthase may not reside in its CO binding site (i.e., heme).

APA, Harvard, Vancouver, ISO, and other styles

5

Edwards, Aurélie, and Thomas L. Pallone. "Mechanisms underlying angiotensin II-induced calcium oscillations." American Journal of Physiology-Renal Physiology 295, no. 2 (August 2008): F568—F584. http://dx.doi.org/10.1152/ajprenal.00107.2008.

Full text

Abstract:

To gain insight into the mechanisms that underlie angiotensin II (ANG II)-induced cytoplasmic Ca2+ concentration ([Ca]cyt) oscillations in medullary pericytes, we expanded a prior model of ion fluxes. ANG II stimulation was simulated by doubling maximal inositol trisphosphate (IP3) production and imposing a 90% blockade of K+ channels. We investigated two configurations, one in which ryanodine receptors (RyR) and IP3 receptors (IP3R) occupy a common store and a second in which they reside on separate stores. Our results suggest that Ca2+ release from stores and import from the extracellular space are key determinants of oscillations because both raise [Ca] in subplasmalemmal spaces near RyR. When the Ca2+-induced Ca2+ release (CICR) threshold of RyR is exceeded, the ensuing Ca2+ release is limited by Ca2+ reuptake into stores and export across the plasmalemma. If sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) pumps do not remain saturated and sarcoplasmic reticulum Ca2+ stores are replenished, that phase is followed by a resumption of leak from internal stores that leads either to [Ca]cyt elevation below the CICR threshold (no oscillations) or to elevation above it (oscillations). Our model predicts that oscillations are more prone to occur when IP3R and RyR stores are separate because, in that case, Ca2+ released by RyR during CICR can enhance filling of adjacent IP3 stores to favor a high subsequent leak that generates further CICR events. Moreover, the existence or absence of oscillations depends on the set points of several parameters, so that biological variation might well explain the presence or absence of oscillations in individual pericytes.

APA, Harvard, Vancouver, ISO, and other styles

6

Leckenby, Simon, and Timothy Chimunda. "Terlipressin rescue therapy in renin-aldosterone-angiotensin system dysregulation induced shock." Australian Critical Care 33 (2020): S35. http://dx.doi.org/10.1016/j.aucc.2020.04.110.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Gur, Yael, Haim Breitbart, Yehudit Lax, Sara Rubinstein, and Nadav Zamir. "Angiotensin II induces acrosomal exocytosis in bovine spermatozoa." American Journal of Physiology-Endocrinology and Metabolism 275, no. 1 (July 1, 1998): E87—E93. http://dx.doi.org/10.1152/ajpendo.1998.275.1.e87.

Full text

Abstract:

Ejaculated mammalian spermatozoa must reside in the female genital tract for some time before gaining the ability to fertilize the egg. During this time, spermatozoa undergo some physiological changes that collectively are called capacitation. Capacitation of mammalian spermatozoa is a prerequisite for acrosome reaction, which is an exocytotic event occurring before fertilization. The specific biophysical and biochemical changes that accompany sperm capacitation and the agonists inducing acrosome reaction are not fully understood. Using SDS-gel electrophoresis and immunoblotting, we demonstrate the existence of a class of angiotensin receptors (AT1) in bovine spermatozoa. In capacitated sperm, we show that angiotensin II (ANG II) AT1 receptors are localized in the head and tail, whereas in noncapacitated cells the receptors are localized in the tail only. We find that ANG II markedly stimulates acrosomal exocytosis of capacitated bovine spermatozoa in vitro in a concentration range of 0.1–10 nM. No effect of ANG II was found in noncapacitated cells. The ability of ANG II to stimulate the acrosome reaction depends on the presence of calcium ions in the incubation medium. The ANG II-induced acrosome reaction was markedly inhibited by a selective AT1 receptor antagonist, losartan (DUP 753). PD-123319, a selective antagonist of the ANG II AT2 receptor, had no effect on the ANG II-induced acrosome reaction. Thus ANG II via activation of AT1 receptors may play a regulatory role in the induction of the acrosome reaction.

APA, Harvard, Vancouver, ISO, and other styles

8

Lee, Shin-Hann, Sarah M. Gomes, Judy Ghalayini, Konstantin G. Iliadi, and Gabrielle L. Boulianne. "Angiotensin Converting Enzyme Inhibitors and Angiotensin Receptor Blockers Rescue Memory Defects in Drosophila-Expressing Alzheimer’s Disease-Related Transgenes Independently of the Canonical Renin Angiotensin System." eneuro 7, no. 6 (October 15, 2020): ENEURO.0235–20.2020. http://dx.doi.org/10.1523/eneuro.0235-20.2020.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Sun, Bei, Jonathan S. Williams, Luminita Pojoga, Bindu Chamarthi, Jessica Lasky-Su, Benjamin A. Raby, Paul N. Hopkins, et al. "Renin gene polymorphism: its relationship to hypertension, renin levels and vascular responses." Journal of the Renin-Angiotensin-Aldosterone System 12, no. 4 (April 13, 2011): 564–71. http://dx.doi.org/10.1177/1470320311405873.

Full text

Abstract:

The renin gene has been previously reported to be associated with essential hypertension in a variety of ethnic groups. However, no studies have systematically evaluated the relationship between single nucleotide polymorphisms (SNPs) representing coverage of the entire renin gene and hypertension risk. To evaluate the association between renin gene variation and hypertension we investigated data on HyperPATH cohort with 570 hypertensive and 222 normotensive Caucasian subjects. Six tagging SNPs and resultant haplotypes were tested for associations with hypertension risk, followed by mean arterial pressure (MAP), plasma renin activity (PRA) and the change in MAP in response to angiotensin II (AngII) infusion (AngII ΔMAP). The A allele of SNP rs6693954 and the haplotype containing rs6696954A were significantly associated with higher risk for hypertension (OR = 1.98, p = 0.0001; OR = 1.63 p = 0.0005, respectively). The same haplotype block was also associated with altered PRA levels and blunted AngII ΔMAP (global p-value = 0.02, 0.047, respectively). Our results confirm that polymorphisms in the renin gene are associated with increased risk for hypertension in an independent cohort, and that the underlying mechanism may reside in the interaction of renin activity and vascular responsiveness to angiotensin II.

APA, Harvard, Vancouver, ISO, and other styles

10

Royea, Jessika, Maria Lacalle-Aurioles, Lianne J. Trigiani, Alice Fermigier, and Edith Hamel. "AT2R’s (Angiotensin II Type 2 Receptor’s) Role in Cognitive and Cerebrovascular Deficits in a Mouse Model of Alzheimer Disease." Hypertension 75, no. 6 (June 2020): 1464–74. http://dx.doi.org/10.1161/hypertensionaha.119.14431.

Full text

Abstract:

Antihypertensive medications targeting the renin-angiotensin system have lowered the incidence and progression of Alzheimer disease. Understanding how these medications function could lead to novel therapeutic strategies. AT4Rs (angiotensin IV receptors) have been associated with angiotensin receptor blockers’ cognitive, cerebrovascular, and neuroinflammatory rescue in Alzheimer disease models. Yet, whether AT4Rs act alone or with AT2Rs remains unknown. Here, we investigated whether AT2Rs contribute to losartan’s benefits and whether chronic AT2R activation could mimic angiotensin receptor blocker benefits in transgenic mice overexpressing familial Alzheimer disease mutations of the human APP (amyloid precursor protein). Losartan-treated mice (10 mg/kg per day, drinking water, 7 months) received intracerebroventricular (1 month) administration of vehicle or AT2R antagonist PD123319 (1.6 nmol/day). PD123319 countered losartan’s benefits on spatial learning and memory, neurovascular coupling, and hampered those on oxidative stress and nitric oxide bioavailability. PD123319 did not oppose losartan’s benefits on short-term memory and vasodilatory function and had no benefit on neuroinflammation or Aβ (amyloid β) pathology. Mice receiving either vehicle or selective AT2R agonist compound 21 (intracerebroventricular: 1 nmol/day, 1 month or drinking water: 10 mg/kg per day, 7 months), showed no improvement in memory, vasodilatory function, or nitric oxide bioavailability. Compound 21 treatment normalized neurovascular coupling, reduced astrogliosis independent of persisting microgliosis, and exacerbated oxidative stress in APP mice. Compound 21 reduced dense core Aβ plaques, but not diffuse plaques or Aβ species. Our findings suggest that targeting AT2Rs is not an ideal strategy for restoring Aβ-related cognitive and cerebrovascular deficits.

APA, Harvard, Vancouver, ISO, and other styles

11

Fitts, D. A. "Angiotensin II receptors in SFO but not in OVLT mediate isoproterenol-induced thirst." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 1 (July 1, 1994): R7—R15. http://dx.doi.org/10.1152/ajpregu.1994.267.1.r7.

Full text

Abstract:

Thirst elicited by the beta-adrenergic agonist isoproterenol in rats depends in part on the secretion of renin, the consequent synthesis of angiotensin II (ANG II), and the binding of circulating ANG II to dipsogenic receptors in the brain. These receptors probably reside in either of two forebrain circumventricular organs, the subfornical organ (SFO) or organum vasculosum laminae terminalis (OVLT). Experiments determined that lesions of the SFO, but not of the OVLT, reduced drinking induced by isoproterenol treatment. Competitive ANG II-receptor antagonism with sarthran reduced isoproterenol-induced drinking when the blocker was infused into the SFO but not when it was infused into the OVLT or into the lateral ventricles at a 25-fold greater dose. The findings confirm the widely held belief that renin-dependent thirst elicited by isoproterenol relies on ANG II binding to receptor sites at a circumventricular organ in the brain. The results demonstrate that this site is the SFO and not the OVLT.

APA, Harvard, Vancouver, ISO, and other styles

12

Yvan-Charvet, Laurent, Florence Massiéra, Noël Lamandé, Gérard Ailhaud, Michèle Teboul, Naima Moustaid-Moussa, Jean-Marie Gasc, and Annie Quignard-Boulangé. "Deficiency of Angiotensin Type 2 Receptor Rescues Obesity But Not Hypertension Induced by Overexpression of Angiotensinogen in Adipose Tissue." Endocrinology 150, no. 3 (October 23, 2008): 1421–28. http://dx.doi.org/10.1210/en.2008-1120.

Full text

Abstract:

Increased angiotensinogen (AGT) production by white adipose tissue has been related to not only obesity but also hypertension. Several studies have highlighted the importance of the angiotensin II type 2 receptor (AT2) in the regulation of blood pressure and fat mass, but the relevance of this transporter in a physiopathological model of increased AGT production, as it occurs in obesity, has not yet been investigated. We used transgenic mice that display either a deletion of AT2 (AT2 KO), an overexpression of AGT (OVEX), or both compound mutants (KOVEX). Results demonstrated that adipocyte hypertrophy and increased lipogenic gene expression induced by adipose AGT overproduction was rescued by deletion of AT2. In line with AGT overexpression, KOVEX and OVEX mice have similar increased plasma AGT levels. However, KOVEX mice display a higher blood pressure than OVEX mice. In kidney, renin expression was clearly reduced in OVEX mice, and its expression was normalized in KOVEX mice. Taken together, we demonstrated that the loss of AT2 expression was sufficient to rescue obesity induced by adipose tissue AGT overexpression and confirmed the necessary role of AT2 for the onset of obesity in this model. Furthermore, despite a reduction of adipose mass in KOVEX, AT2 deficiency caused increased renin production, further worsening the hypertension caused by AGT overexpression. Angiotensin type 2 receptor shows antihypertensive function but promotes the angiotensin II-mediated fat mass enlargement.

APA, Harvard, Vancouver, ISO, and other styles

13

He, Hongli, Ling Liu, Qihong Chen, Airan Liu, Shixia Cai, Yi Yang, Xiaomin Lu, and Haibo Qiu. "Mesenchymal Stem Cells Overexpressing Angiotensin-Converting Enzyme 2 Rescue Lipopolysaccharide-Induced Lung Injury." Cell Transplantation 24, no. 9 (September 2015): 1699–715. http://dx.doi.org/10.3727/096368914x685087.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Easterling, T. "Low-dose, short-acting, angiotensin-converting enzyme inhibitors as rescue therapy in pregnancy." Obstetrics & Gynecology 96, no. 6 (December 2000): 956–61. http://dx.doi.org/10.1016/s0029-7844(00)01037-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

PRYDE, P. "Low-dose, short-acting, angiotensin-converting enzyme inhibitors as rescue therapy in pregnancy." Obstetrics & Gynecology 97, no. 5 (May 2001): 799. http://dx.doi.org/10.1016/s0029-7844(01)01371-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

EASTERLING, THOMAS R., DARCY B. CARR, CONNIE DAVIS, CYDNEY DIEDERICHS, DEBRA A. BRATENG, and BARBARA SCHMUCKER. "Low-Dose, Short-Acting, Angiotensin-Converting Enzyme Inhibitors as Rescue Therapy in Pregnancy." Obstetrics & Gynecology 96, no. 6 (December 2000): 956–61. http://dx.doi.org/10.1097/00006250-200012000-00017.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Pryde, Peter G., and Mason Barr. "LOW-DOSE, SHORT-ACTING,ANGIOTENSIN-CONVERTING ENZYME INHIBITORS AS RESCUE THERAPY IN PREGNANCY." Obstetrics & Gynecology 97, no. 5 (May 2001): 799. http://dx.doi.org/10.1097/00006250-200105000-00031.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Easterling, Thomas R. "LOW-DOSE, SHORT-ACTING,ANGIOTENSIN-CONVERTING ENZYME INHIBITORS AS RESCUE THERAPY IN PREGNANCY." Obstetrics & Gynecology 97, no. 5 (May 2001): 799–800. http://dx.doi.org/10.1097/00006250-200105000-00032.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Funk, Steven D., Raymond H. Bayer, and Jeffrey H. Miner. "Endothelial cell-specific collagen type IV-α3expression does not rescue Alport syndrome inCol4a3−/−mice." American Journal of Physiology-Renal Physiology 316, no. 5 (May 1, 2019): F830—F837. http://dx.doi.org/10.1152/ajprenal.00556.2018.

Full text

Abstract:

The glomerular basement membrane (GBM) is a critical component of the kidney’s blood filtration barrier. Alport syndrome, a hereditary disease leading to kidney failure, is caused by the loss or dysfunction of the GBM’s major collagen type IV (COL4) isoform α3α4α5. The constituent COL4 α-chains assemble into heterotrimers in the endoplasmic reticulum before secretion into the extracellular space. If any one of the α3-, α4-, or α5-chains is lost due to mutation of one of the genes, then the entire heterotrimer is lost. Patients with Alport syndrome typically have mutations in the X-linked COL4A5 gene or uncommonly have the autosomal recessive form of the disease due to COL4A3 or COL4A4 mutations. Treatment for Alport syndrome is currently limited to angiotensin-converting enzyme inhibition or angiotensin receptor blockers. Experimental approaches in Alport mice have demonstrated that induced expression of COL4A3, either widely or specifically in podocytes of Col4a3−/−mice, can abrogate disease progression even after establishment of the abnormal GBM. While targeting podocytes in vivo for gene therapy is a significant challenge, the more accessible glomerular endothelium could be amenable for mutant gene repair. In the present study, we expressed COL4A3 in Col4a3−/−Alport mice using an endothelial cell-specific inducible transgenic system, but collagen-α3α4α5(IV) was not detected in the GBM or elsewhere, and the Alport phenotype was not rescued. Our results suggest that endothelial cells do not express the Col4a3/a4/a5 genes and should not be viewed as a target for gene therapy.

APA, Harvard, Vancouver, ISO, and other styles

20

Kule, Chris E., Vijaya Karoor, Jonathan N. E. Day, Walter G. Thomas, Kenneth M. Baker, Kathleen A. Acker, and George W. Booz. "1029-176 Rescue of internalization-impaired angiotensin II AT1 mutants by β-arrestin overexpression." Journal of the American College of Cardiology 43, no. 5 (March 2004): A455—A456. http://dx.doi.org/10.1016/s0735-1097(04)91923-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Santos, Edson L., Rosana I. Reis, Ronaldo G. Silva, Suma I. Shimuta, Christiane Pecher, Jean-Loup Bascands, Joost P. Schanstra, et al. "Functional rescue of a defective angiotensin II AT1 receptor mutant by the Mas protooncogene." Regulatory Peptides 141, no. 1-3 (June 2007): 159–67. http://dx.doi.org/10.1016/j.regpep.2006.12.030.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Robert, Martine, David De Bels, Martin Chaumont, Patrick M. Honoré, and Philippe Gottignies. "Angiotensin converting enzyme inhibitor intoxication: Naloxone to the rescue? Naloxone for ACE inhibitor intoxication." American Journal of Emergency Medicine 37, no. 6 (June 2019): 1217.e1–1217.e2. http://dx.doi.org/10.1016/j.ajem.2019.03.046.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Poulsen, Knud, Arne Høj Nielsen, and Arne Johannessen. "Measurement of inactive renin in normal, nephrectomized, and adrenalectomized rats." Canadian Journal of Physiology and Pharmacology 69, no. 9 (September 1, 1991): 1381–84. http://dx.doi.org/10.1139/y91-205.

Full text

Abstract:

In a new method for measurement of inactive rat plasma renin, the trypsin generated angiotensin I immunoreactive material, which was HPLC characterized as similar to tetradecapeptide renin substrate, is removed by a cation exchange resin before the renin incubation step. The method also corrects for trypsin destruction of endogenous angiotensinogen by the addition of exogenous angiotensinogen. When measured with this method inactive renin in rat plasma decreased after nephrectomy and increased after adrenalectomy. This is in accordance with findings in humans. A sexual dimorphism of prorenin (inactive renin) in rat plasma, similar to that reported in humans and mice, was demonstrated. Thus, inactive renin in the rat is no exception among species, and the rat might be a suitable animal model for further studies dealing with the physiology of prorenin in plasma and tissues.Key words: angiotensinogen, inactive renin, renin.

APA, Harvard, Vancouver, ISO, and other styles

24

Bridgeman, Mary Barna, Milisha Shah, and Edward Foote. "Potassium-lowering agents for the treatment of nonemergent hyperkalemia: pharmacology, dosing and comparative efficacy." Nephrology Dialysis Transplantation 34, Supplement_3 (December 1, 2019): iii45—iii50. http://dx.doi.org/10.1093/ndt/gfz223.

Full text

Abstract:

Abstract Hyperkalemia represents a common and potentially life-threating electrolyte abnormality, a complication frequently observed in patients with heart failure, kidney disease, diabetes or in those receiving drug therapies influencing the renin–angiotensin–aldosterone system. Elevated serum potassium levels are often the result of impaired urinary potassium elimination, inadequate or reduced cellular potassium uptake, severe heart failure, use of medications influencing potassium levels in the circulation, or, more commonly, a combination of these factors. Strategies for the treatment of nonemergent hyperkalemia include the use of cation-exchange resins, polymers or other novel mechanisms of potassium trapping, including sodium polystyrene sulfonate, patiromer and sodium zirconium cyclosilicate. These agents differ in their pharmacology and mechanism of action, clinical efficacy, including onset and extent of potassium-lowering effect, dosage and administration, and potential safety and adverse effect profiles. In this review, an evaluation of these characteristics, including clinical evidence and safety concerns, in the management of nonemergent hyperkalemia will be explored.

APA, Harvard, Vancouver, ISO, and other styles

25

Lakhani, Hari Vishal, Mishghan Zehra, Sneha S. Pillai, Nitin Puri, Joseph I. Shapiro, Nader G. Abraham, and Komal Sodhi. "Beneficial Role of HO-1-SIRT1 Axis in Attenuating Angiotensin II-Induced Adipocyte Dysfunction." International Journal of Molecular Sciences 20, no. 13 (June 29, 2019): 3205. http://dx.doi.org/10.3390/ijms20133205.

Full text

Abstract:

Background: Angiotensin II (Ang II), released by the renin–angiotensin–aldosterone system (RAAS), contributes to the modulatory role of the RAAS in adipose tissue dysfunction. Investigators have shown that inhibition of AngII improved adipose tissue function and insulin resistance in mice with metabolic syndrome. Heme Oxygenase-1 (HO-1), a potent antioxidant, has been demonstrated to improve oxidative stress and adipocyte phenotype. Molecular effects of high oxidative stress include suppression of sirtuin-1 (SIRT1), which is amenable to redox manipulations. The mechanisms involved, however, in these metabolic effects of the RAAS remain incompletely understood. Hypothesis: We hypothesize that AngII-induced oxidative stress has the potential to suppress adipocyte SIRT1 via down regulation of HO-1. This effect of AngII will, in turn, upregulate mineralocorticoid receptor (MR). The induction of HO-1 will rescue SIRT1, hence improving oxidative stress and adipocyte phenotype. Methods and Results: We examined the effect of AngII on lipid accumulation, oxidative stress, and inflammatory cytokines in mouse pre-adipocytes in the presence and absence of cobalt protoporphyrin (CoPP), HO-1 inducer, tin mesoporphyrin (SnMP), and HO-1 inhibitor. Our results show that treatment of mouse pre-adipocytes with AngII increased lipid accumulation, superoxide levels, inflammatory cytokine levels, interleukin-6 (IL-6) and tumor necrosis factor α (TNFα), and adiponectin levels. This effect was attenuated by HO-1 induction, which was further reversed by SnMP, suggesting HO-1 mediated improvement in adipocyte phenotype. AngII-treated pre-adipocytes also showed upregulated levels of MR and suppressed SIRT1 that was rescued by HO-1. Subsequent treatment with CoPP and SIRT1 siRNA in mouse pre-adipocytes increased lipid accumulation and fatty acid synthase (FAS) levels, suggesting that beneficial effects of HO-1 are mediated via SIRT1. Conclusion: Our study demonstrates for the first time that HO-1 has the ability to restore cellular redox, rescue SIRT1, and prevent AngII-induced impaired effects on adipocytes and the systemic metabolic profile.

APA, Harvard, Vancouver, ISO, and other styles

26

EASTERLING, T. "Low-dose, short-acting, angiotensin-converting enzyme inhibitors as rescue therapy in pregnancy: In reply." Obstetrics & Gynecology 97, no. 5 (May 2001): 799–800. http://dx.doi.org/10.1016/s0029-7844(01)01391-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Manley-Casco, Dario, and Paul Berkowitz. "A Whole Food Plant-Based Diet With a Novel Potassium-Binding Resin in a Patient With Advanced Chronic Kidney Disease." American Journal of Lifestyle Medicine 14, no. 6 (August 29, 2020): 592–94. http://dx.doi.org/10.1177/1559827620951036.

Full text

Abstract:

Chronic kidney disease (CKD) is a major health problem with substantial morbidity and mortality. Plant-based diets decrease the incidence of CKD and progression of kidney disease and help prevent and treat the important comorbidities of obesity, type 2 diabetes, hypertension, and cardiovascular disease. However, in patients with CKD, there is concern that a plant-based diet may contribute to life-threatening hyperkalemia. We present a patient with CKD secondary to hypertensive glomerulosclerosis that worsened despite standard of care treatment. Shared decision making was used to initiate a whole food plant-based diet along with a potassium-binding resin (Patiromer) to control the potassium levels. The patient was able to be maintained on the whole food plant-based diet and an angiotensin-converting enzyme inhibitor without the development of hyperkalemia. This case shows that patients with CKD may be able to enjoy the benefits of a whole food plant-based diet while decreasing the risk of hyperkalemia by using the new potassium binders.

APA, Harvard, Vancouver, ISO, and other styles

28

Sharma, Ravindra K., Aline C. Oliveira, Tao Yang, Marianthi M. Karas, Jing Li, Gilberto O. Lobaton, Victor P. Aquino, et al. "Gut Pathology and Its Rescue by ACE2 (Angiotensin-Converting Enzyme 2) in Hypoxia-Induced Pulmonary Hypertension." Hypertension 76, no. 1 (July 2020): 206–16. http://dx.doi.org/10.1161/hypertensionaha.120.14931.

Full text

Abstract:

Therapeutic advances for pulmonary hypertension (PH) have been incremental because of the focus on the pulmonary vasculature in PH pathology. Here, we evaluate the concept that PH is, rather, a systemic disorder involving interplay among multiorgan systems, including brain, gut, and lungs. Therefore, the objective of this study was to evaluate the hypothesis that PH is associated with a dysfunctional brain-gut-lung axis and that global overexpression of ACE2 (angiotensin-converting enzyme 2) rebalances this axis and protects against PH. ACE2 knockin and wild-type (WT; C57BL/6) mice were subjected to chronic hypoxia (10% FIO2) or room air for 4 weeks. Cardiopulmonary hemodynamics, histology, immunohistochemistry, and fecal 16S rRNA microbial gene analyses were evaluated. Hypoxia significantly increased right ventricular systolic pressure, sympathetic activity as well as the number and activation of microglia in the paraventricular nucleus of the hypothalamus in WT mice. This was associated with a significant increase in muscularis layer thickening and decreases in both villi length and goblet cells and altered gut microbiota. Global overexpression of ACE2 prevented changes in hypoxia-induced pulmonary and gut pathophysiology and established distinct microbial communities from WT hypoxia mice. Furthermore, WT mice subjected to fecal matter transfer from ACE2 knockin mice were resistant to hypoxia-induced PH compared with their controls receiving WT fecal matter transfer. These observations demonstrate that ACE2 ameliorates these hypoxia-induced pathologies and attenuates PH. The data implicate dysfunctional brain-gut-lung communication in PH and provide novel avenues for therapeutic interventions.

APA, Harvard, Vancouver, ISO, and other styles

29

HALLINAN, E. ANN. "Formation of a dehydroalanyl residue from S-benzylcysteine upon HF cleavage of a [Sar1, Cys8]-angiotensin II peptide resin." International Journal of Peptide and Protein Research 38, no. 6 (January 12, 2009): 601–2. http://dx.doi.org/10.1111/j.1399-3011.1991.tb01546.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Langeveld, B. E., R. H. Henning, B. J. G. L. de Smet, F. Zijlstra, A. Driessen, E. Tijsma, W. H. van Gilst, and A. J. M. Roks. "Rescue of arterial function by angiotensin-(1-7): towards improvement of endothelial function by drug-eluting stents." Netherlands Heart Journal 16, no. 9 (September 2008): 293–98. http://dx.doi.org/10.1007/bf03086167.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Vashistha, Himanshu, Pravin C. Singhal, Ashwani Malhotra, Mohammad Husain, Peter Mathieson, Moin A. Saleem, Cyril Kuriakose, et al. "Null mutations at the p66 and bradykinin 2 receptor loci induce divergent phenotypes in the diabetic kidney." American Journal of Physiology-Renal Physiology 303, no. 12 (December 15, 2012): F1629—F1640. http://dx.doi.org/10.1152/ajprenal.00246.2012.

Full text

Abstract:

Candidate genes have been identified that confer increased risk for diabetic glomerulosclerosis (DG). Mice heterozygous for the Akita (Ins2+/C96Y) diabetogenic mutation with a second mutation introduced at the bradykinin 2 receptor (B2R−/−) locus express a disease phenotype that approximates human DG. Src homology 2 domain transforming protein 1 (p66) controls mitochondrial metabolism and cellular responses to oxidative stress, aging, and apoptosis. We generated p66-null Akita mice to test whether inactivating mutations at the p66 locus will rescue kidneys of Akita mice from disease-causing mutations at the Ins2 and B2R loci. Here we show null mutations at the p66 and B2R loci interact with the Akita (Ins2+/C96Y) mutation, independently and in combination, inducing divergent phenotypes in the kidney. The B2R−/− mutation induces detrimental phenotypes, as judged by increased systemic and renal levels of oxidative stress, histology, and urine albumin excretion, whereas the p66-null mutation confers a powerful protection phenotype. To elucidate the mechanism(s) of the protection phenotype, we turned to our in vitro system. Experiments with cultured podocytes revealed previously unrecognized cross talk between p66 and the redox-sensitive transcription factor p53 that controls hyperglycemia-induced ROS metabolism, transcription of p53 target genes (angiotensinogen, angiotensin II type-1 receptor, and bax), angiotensin II generation, and apoptosis. RNA-interference targeting p66 inhibits all of the above. Finally, protein levels of p53 target genes were upregulated in kidneys of Akita mice but unchanged in p66-null Akita mice. Taken together, p66 is a potential molecular target for therapeutic intervention in DG.

APA, Harvard, Vancouver, ISO, and other styles

32

Zhang, Fengxiang, Zhang Wang, and Shiying Xu. "Macroporous resin purification of grass carp fish (Ctenopharyngodon idella) scale peptides with in vitro angiotensin-I converting enzyme (ACE) inhibitory ability." Food Chemistry 117, no. 3 (December 2009): 387–92. http://dx.doi.org/10.1016/j.foodchem.2009.04.015.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Gao, Xiujun, Xiqi Li, Peisheng Yan, Rui Sun, Guangfeng Kan, and Ying Zhou. "Identification and Functional Mechanism of Novel Angiotensin I Converting Enzyme Inhibitory Dipeptides from Xerocomus badius Cultured in Shrimp Processing Waste Medium." BioMed Research International 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/5089270.

Full text

Abstract:

ACE inhibitory dipeptides from Xerocomus badius fermented shrimp processing waste were isolated with ethanol, macroporous resin, chloroform, and Sephadex G-10 in sequence and identified by LC-MS/MS system coupled with electrospray ionization source. Molecular docking was performed for exploring the mechanism of their inhibitions. The results showed that the identified ACE inhibitory dipeptides were Cys-Cys and Cys-Arg with IC50 values of 4.37 ± 0.07 and 475.95 ± 0.11 μM, respectively. The difference between ACE inhibitor potency of Cys-Cys and Cys-Arg could be explained by results of molecular docking. Cys-Cys formed crucial coordination between carboxyl oxygen and Zn(II), hydrogen bonds with residues Ala354(O), Ala356(HN), and Tyr523(OH), and a bump with the residue His387(NE2) at the active site of ACE. There was no coordination, except for 5 hydrogen bonds (at residues His353, Ala354, Glu384, Glu403, and Arg522) and a bump (Glu411) between Cys-Arg and active site of ACE. These findings highlighted that Cys-Cys could be considered as a novel potent ACE inhibitor, and coordination between its carboxyl oxygen and Zn(II) played significant role in defining its ACE inhibitor potency.

APA, Harvard, Vancouver, ISO, and other styles

34

Barreto-Chaves, M. L., and M. Mello-Aires. "Effect of luminal angiotensin II and ANP on early and late cortical distal tubule HCO3- reabsorption." American Journal of Physiology-Renal Physiology 271, no. 5 (November 1, 1996): F977—F984. http://dx.doi.org/10.1152/ajprenal.1996.271.5.f977.

Full text

Abstract:

Bicarbonate reabsorption was evaluated by stationary microperfusion “in vivo“ early distal (ED) and late distal (LD) segments of at kidney. Intratubular pH was recorded by double-barreled of H+ exchange resin/reference (1 M KCl) microelectrodes for the determination of HCO3- reabsorption. In the presence of angiotensin II (ANG II) (10(-12) M), a significant increase in HCO3- reabsorption was observed both in ED (from 0.930 +/- 0.060 to 2.64 +/- 0.210 nmol.cm-2.s-1 in luminally perfused tubules and from 0.850 +/- 0.040 to 2.03 +/- 0.210 nmol.cm-2.s-1 during capillary perfusion) and LD segments from 0.310 +/- 0.130 to 2.16 +/- 0.151 nmol.cm-2.s-1 during luminal perfusion and from 0.530 +/- 0.031 to 2.16 +/- 0.211 nmol.cm-2.s-1 with capillary perfusion). The addition of the AT1-receptor antagonist losartan (10(-6) M) to luminal perfusion blocked luminal ANG II-mediated stimulation in ED and LD segments. 5-(N,N-hexamethylene)amiloride (10(-4) M) added to luminal perfusion inhibited luminal ANG II-mediated stimulation in ED (by 81%) and LD (by 54%) segments. The addition of bafilomycin A1 (2 x 10(-7) M) to luminal perfusion does not affect luminal ANG II-mediated stimulation in ED segments but reduces it in LD segments (by 33%). During the addition of atrial natriuretic peptide (ANP) (10(-6) M) or ANG II plus ANP in both segments, no significant differences in HCO3- reabsorption were observed. Our results indicate that luminal ANG II acts to stimulate Na+/H+ exchange in ED and LD segments via activation of AT1 receptors, as well as the vacuolar H(+)-adenosinetriphosphatase in LD segments. ANP does not affect HCO3- reabsorption in either ED or LD segments and does not impair the stimulation caused by ANG II.

APA, Harvard, Vancouver, ISO, and other styles

35

Kanduri, Swetha Rani, Kathryn J. Suchow, and Juan Carlos Q. Velez. "A Rare Case of Patiromer Induced Hypercalcemia." Journal of Clinical Medicine 10, no. 16 (August 23, 2021): 3756. http://dx.doi.org/10.3390/jcm10163756.

Full text

Abstract:

Patiromer is a calcium (Ca)-potassium (K) exchange resin approved for the treatment of hyperkalemia. Disorders of Ca or acid base balance were not reported in pre-approval clinical trials. We present a case of a patient with chronic kidney disease (CKD) with an unusual picture of hypercalcemia, metabolic alkalosis and hypokalemia upon intensification of patiromer dosing. A 56-year-old white man with CKD stage 4 (baseline creatinine 2.8 mg/dL) due to type 1 diabetes mellitus, proteinuria (1.5 g/g) and persistently high serum potassium 5.9 mEq/L attributed to type 4 renal tubular acidosis was evaluated in clinic. Due to high risk of CKD progression, patiromer 8.4 g daily, followed by 16.8 g daily was prescribed to enable renin angiotensin aldosterone system (RAAS) inhibitor. After 5 months of being on patiromer 16.8 g daily, routine laboratory tests revealed serum potassium 2.5 mEq/L, serum calcium 12.8 mg/dL and carbon dioxide 34 mEq/L. Patiromer was discontinued and thorough investigation held was negative for other causes of hypercalcemia. Five days after patiromer discontinuation, serum calcium returned to normal. The role of secondary hyperparathyroidism in this case remains unclear. We, therefore recommend cautious vigilance of patients receiving patiromer and undergoing dose escalation.

APA, Harvard, Vancouver, ISO, and other styles

36

Rubio Campal, José Manuel, Hugo Del Castillo, Belén Arroyo Rivera, Carmen De Juan Bitriá, Mikel Taibo Urquia, Pepa Sánchez Borque, Ángel Miracle Blanco, Loreto Bravo Calero, David Martí Sánchez, and José Tuñón Fernández. "Improvement in quality of life with sacubitril/ /valsartan in cardiac resynchronization non-responders: The RESINA (RESynchronization plus an Inhibitor of Neprilysin/Angiotensin) registry." Cardiology Journal 28, no. 3 (May 25, 2021): 402–10. http://dx.doi.org/10.5603/cj.a2021.0009.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Doyle, M. P., and B. R. Walker. "Attentuation of systemic vasoreactivity in chronically hypoxic rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 6 (June 1, 1991): R1114—R1122. http://dx.doi.org/10.1152/ajpregu.1991.260.6.r1114.

Full text

Abstract:

Experiments were performed to assess the effects of chronic hypoxia on systemic vasoreactivity in conscious unrestrained rats and in abdominal aortic rings. Two groups of rats were used: normoxic controls and chronically hypoxic rats that were maintained in a hypobaric chamber (380 mmHg) for 4 wk before experimentation. In conscious animals instrumented with pulsed Doppler cardiac output probes and arterial and venous catheters, mean arterial pressure and mean cardiac output were measured before and during graded continuous infusions of phenylephrine (PE), angiotensin II, and arginine vasopressin (AVP). Measurements were made while the animals breathed either room air or 12% O2. Acute exposure to 12% O2 significantly reduced pressor and vasoconstrictor responses for all three agents. These responses were also attenuated in the chronically hypoxic rats in 12% O2; however, acute return to room air conditions did not return pressor or vasoconstrictor responses to normoxic control levels. In abdominal aortic rings from both groups of animals, cumulative dose-response curves to PE and AVP were completed in 21 and 3% O2 conditions. Neither acute nor chronic hypoxia caused a shift in the dose-response curves. In rings from control rats, maximum tension responses to AVP were significantly diminished in 3% O2. Rings from chronically hypoxic rats exhibited less maximum tension to AVP in 21% O2 than did rings from control rats. We conclude that acute hypoxia reversibly attenuates systemic vasoreactivity and that chronic hypoxia induces a more sustained decrease in reactivity. In addition, at least part of the mechanism may reside within the vasculature.

APA, Harvard, Vancouver, ISO, and other styles

38

Pawlik, Marek J., Barbara Miziak, Aleksandra Walczak, Agnieszka Konarzewska, Magdalena Chrościńska-Krawczyk, Jan Albrecht, and Stanisław J. Czuczwar. "Selected Molecular Targets for Antiepileptogenesis." International Journal of Molecular Sciences 22, no. 18 (September 8, 2021): 9737. http://dx.doi.org/10.3390/ijms22189737.

Full text

Abstract:

The term epileptogenesis defines the usually durable process of converting normal brain into an epileptic one. The resistance of a significant proportion of patients with epilepsy to the available pharmacotherapy prompted the concept of a causative treatment option consisting in stopping or modifying the progress of epileptogenesis. Most antiepileptic drugs possess only a weak or no antiepileptogenic potential at all, but a few of them appear promising in this regard; these include, for example, eslicarbazepine (a sodium and T-type channel blocker), lamotrigine (a sodium channel blocker and glutamate antagonist) or levetiracetam (a ligand of synaptic vehicle protein SV2A). Among the approved non-antiepileptic drugs, antiepileptogenic potential seems to reside in losartan (a blocker of angiotensin II type 1 receptors), biperiden (an antiparkinsonian drug), nonsteroidal anti-inflammatory drugs, antioxidative drugs and minocycline (a second-generation tetracycline with anti-inflammatory and antioxidant properties). Among other possible antiepileptogenic compounds, antisense nucleotides have been considered, among these an antagomir targeting microRNA-134. The drugs and agents mentioned above have been evaluated in post-status epilepticus models of epileptogenesis, so their preventive efficacy must be verified. Limited clinical data indicate that biperiden in patients with brain injuries is well-tolerated and seems to reduce the incidence of post-traumatic epilepsy. Exceptionally, in this regard, our own original data presented here point to c-Fos as an early seizure duration, but not seizure intensity-related, marker of early epileptogenesis. Further research of reliable markers of early epileptogenesis is definitely needed to improve the process of designing adequate antiepileptogenic therapies.

APA, Harvard, Vancouver, ISO, and other styles

39

Thomas, Walter G., Thomas J. Motel, Christopher E. Kule, Vijay Karoor, and Kenneth M. Baker. "Phosphorylation of the Angiotensin II (AT1A) Receptor Carboxyl Terminus: A Role in Receptor Endocytosis." Molecular Endocrinology 12, no. 10 (October 1, 1998): 1513–24. http://dx.doi.org/10.1210/mend.12.10.0179.

Full text

Abstract:

Abstract The molecular mechanism of angiotensin II type I receptor (AT1) endocytosis is obscure, although the identification of an important serine/threonine rich region (Thr332Lys333Met334Ser335Thr336Leu337Ser338) within the carboxyl terminus of the AT1A receptor subtype suggests that phosphorylation may be involved. In this study, we examined the phosphorylation and internalization of full-length AT1A receptors and compared this to receptors with truncations and mutations of the carboxyl terminus. Epitope-tagged full-length AT1A receptors, when transiently transfected in Chinese hamster ovary (CHO)-K1 cells, displayed a basal level of phosphorylation that was significantly enhanced by angiotensin II (Ang II) stimulation. Phosphorylation of AT1A receptors was progressively reduced by serial truncation of the carboxyl terminus, and truncation to Lys325, which removed the last 34 amino acids, almost completely inhibited Ang II-stimulated 32P incorporation into the AT1A receptor. To investigate the correlation between receptor phosphorylation and endocytosis, an epitope-tagged mutant receptor was produced, in which the carboxyl-terminal residues, Thr332, Ser335, Thr336, and Ser338, previously identified as important for receptor internalization, were substituted with alanine. Compared with the wild-type receptor, this mutant displayed a clear reduction in Ang II-stimulated phosphorylation. Such a correlation was further strengthened by the novel observation that the Ang II peptide antagonist, Sar1Ile8-Ang II, which paradoxically causes internalization of wild-type AT1A receptors, also promoted their phosphorylation. In an attempt to directly relate phosphorylation of the carboxyl terminus to endocytosis, the internalization kinetics of wild-type AT1A receptors and receptors mutated within the Thr332-Ser338 region were compared. The four putative phosphorylation sites (Thr332, Ser335, Thr336, and Ser338) were substituted with either neutral [alanine (A)] or acidic amino acids [glutamic acid (E) and aspartic acid (D)], the former to prevent phosphorylation and the latter to reproduce the acidic charge created by phosphorylation. Wild-type AT1A receptors, expressed in Chinese hamster ovary cells, rapidly internalized after Ang II stimulation [t1/2 2.3 min; maximal level of internalization (Ymax) 78.2%], as did mutant receptors carrying single acidic substitutions (T332E, t1/2 2.7 min, Ymax 76.3%; S335D, t1/2 2.4 min, Ymax 76.7%; T336E, t1/2 2.5 min, Ymax 78.2%; S338D, t1/2 2.6 min, Ymax 78.4%). While acidic amino acid substitutions may simply be not as structurally disruptive as alanine mutations, we interpret the tolerance of a negative charge in this region as suggestive that phosphorylation may permit maximal internalization. Substitution of all four residues to alanine produced a receptor with markedly reduced internalization kinetics (T332A/S335A/T336A/S338A, t1/2 10.1 min, Ymax 47.9%), while endocytosis was significantly rescued in the corresponding quadruple acidic mutant (T332E/S335D/T336E/S338D, t1/2 6.4 min, Ymax 53.4%). Double mutation of S335 and T336 to alanine also diminished the rate and extent of endocytosis (S335A/T336A, 3.9 min, Ymax 69.3%), while the analogous double acidic mutant displayed wild type-like endocytotic parameters (S335D/T336E, t1/2 2.6 min, Ymax 77.5%). Based on the apparent rescue of internalization by acidic amino acid substitutions in a region that we have identified as a site of Ang II-induced phosphorylation, we conclude that maximal endocytosis of the AT1A receptor requires phosphorylation within this serine/threonine-rich segment of the carboxyl terminus.

APA, Harvard, Vancouver, ISO, and other styles

40

Li, Xiao C., Gary E. Shull, Elisa Miguel-Qin, Fang Chen, and Jia L. Zhuo. "Role of the Na+ /H+ exchanger 3 in angiotensin II-induced hypertension in NHE3-deficient mice with transgenic rescue of NHE3 in small intestines." Physiological Reports 3, no. 11 (November 2015): e12605. http://dx.doi.org/10.14814/phy2.12605.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Liu, Peidang, Xiuying Bai, Heming Wang, Andrew Karaplis, David Goltzman, and Dengshun Miao. "Hypophosphatemia-mediated hypotension in transgenic mice overexpressing human FGF-23." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 4 (October 2009): H1514—H1520. http://dx.doi.org/10.1152/ajpheart.00581.2009.

Full text

Abstract:

Fibroblast growth factor-23 (FGF-23) is a potent circulating phosphaturic factor associated with renal phosphate wasting. The effects of FGF-23 on skeletal and phosphate homeostasis have been investigated widely; however, the effect of FGF-23 on the cardiovascular system (CVS) is unknown. To assess whether FGF-23 influences the function and structure of the CVS and whether the effect of FGF-23 on the CVS is mediated by FGF receptors directly or indirectly by hypophosphatemia, FGF-23 transgenic mice and their wild-type littermates were fed a normal diet or a high-phosphate diet comprising a normal diet plus 1.25% phosphate in drinking water from weaning for 5 wk, and the phenotypes of the CVS were compared between FGF-23 transgenic mice and their wild-type littermates on the same diet. At the end of this time period, transgenic animals on the normal diet developed hypotension. The left ventricle was appropriately hypertrophic, and plasma catecholamine and renin-angiotensin system components were upregulated, indicating compensatory mechanisms in response to the hypotension. Transgenic mice also exhibited an impaired vascular reactivity and a downregulation of vasoconstrictor receptor gene expression, possibly as pathogenetic factors contributing to the hypotension. The high-phosphate diet improved the hypophosphatemia, resulting in a rescue of the cardiovascular phenotype. This study demonstrates that FGF-23 overexpression can result in abnormalities in the CVS and that the effect of FGF-23 overexpression on the CVS is mediated by the secondary severe hypophosphatemia.

APA, Harvard, Vancouver, ISO, and other styles

42

Yosri, Nermeen, Aida A. Abd El-Wahed, Reem Ghonaim, Omar M. Khattab, Aya Sabry, Mahmoud A. A. Ibrahim, Mahmoud F. Moustafa, et al. "Anti-Viral and Immunomodulatory Properties of Propolis: Chemical Diversity, Pharmacological Properties, Preclinical and Clinical Applications, and In Silico Potential against SARS-CoV-2." Foods 10, no. 8 (July 31, 2021): 1776. http://dx.doi.org/10.3390/foods10081776.

Full text

Abstract:

Propolis, a resin produced by honeybees, has long been used as a dietary supplement and folk remedy, and more recent preclinical investigations have demonstrated a large spectrum of potential therapeutic bioactivities, including antioxidant, antibacterial, anti-inflammatory, neuroprotective, immunomodulatory, anticancer, and antiviral properties. As an antiviral agent, propolis and various constituents have shown promising preclinical efficacy against adenoviruses, influenza viruses, respiratory tract viruses, herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2), human immunodeficiency virus (HIV), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Over 300 chemical components have been identified in propolis, including terpenes, flavonoids, and phenolic acids, with the specific constituent profile varying widely according to geographic origin and regional flora. Propolis and its constituents have demonstrated potential efficacy against SARS-CoV-2 by modulating multiple pathogenic and antiviral pathways. Molecular docking studies have demonstrated high binding affinities of propolis derivatives to multiple SARS-CoV-2 proteins, including 3C-like protease (3CLpro), papain-like protease (PLpro), RNA-dependent RNA polymerase (RdRp), the receptor-binding domain (RBD) of the spike protein (S-protein), and helicase (NSP13), as well as to the viral target angiotensin-converting enzyme 2 (ACE2). Among these compounds, retusapurpurin A has shown high affinity to 3CLpro (ΔG = −9.4 kcal/mol), RdRp (−7.5), RBD (−7.2), NSP13 (−9.4), and ACE2 (−10.4) and potent inhibition of viral entry by forming hydrogen bonds with amino acid residues within viral and human target proteins. In addition, propolis-derived baccharin demonstrated even higher binding affinity towards PLpro (−8.2 kcal/mol). Measures of drug-likeness parameters, including metabolism, distribution, absorption, excretion, and toxicity (ADMET) characteristics, also support the potential of propolis as an effective agent to combat COVID-19.

APA, Harvard, Vancouver, ISO, and other styles

43

Andrukhova, Olena, Svetlana Slavic, Ute Zeitz, Sabine C. Riesen, Monika S. Heppelmann, Tamas D. Ambrisko, Mato Markovic, Wolfgang M. Kuebler, and Reinhold G. Erben. "Vitamin D Is a Regulator of Endothelial Nitric Oxide Synthase and Arterial Stiffness in Mice." Molecular Endocrinology 28, no. 1 (January 1, 2014): 53–64. http://dx.doi.org/10.1210/me.2013-1252.

Full text

Abstract:

Abstract The vitamin D hormone 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3] is essential for the preservation of serum calcium and phosphate levels but may also be important for the regulation of cardiovascular function. Epidemiological data in humans have shown that vitamin D insufficiency is associated with hypertension, left ventricular hypertrophy, increased arterial stiffness, and endothelial dysfunction in normal subjects and in patients with chronic kidney disease and type 2 diabetes. However, the pathophysiological mechanisms underlying these associations remain largely unexplained. In this study, we aimed to decipher the mechanisms by which 1,25(OH)2D3 may regulate systemic vascular tone and cardiac function, using mice carrying a mutant, functionally inactive vitamin D receptor (VDR). To normalize calcium homeostasis in VDR mutant mice, we fed the mice lifelong with the so-called rescue diet enriched with calcium, phosphate, and lactose. Here, we report that VDR mutant mice are characterized by lower bioavailability of the vasodilator nitric oxide (NO) due to reduced expression of the key NO synthesizing enzyme, endothelial NO synthase, leading to endothelial dysfunction, increased arterial stiffness, increased aortic impedance, structural remodeling of the aorta, and impaired systolic and diastolic heart function at later ages, independent of changes in the renin-angiotensin system. We further demonstrate that 1,25(OH)2D3 is a direct transcriptional regulator of endothelial NO synthase. Our data demonstrate the importance of intact VDR signaling in the preservation of vascular function and may provide a mechanistic explanation for epidemiological data in humans showing that vitamin D insufficiency is associated with hypertension and endothelial dysfunction.

APA, Harvard, Vancouver, ISO, and other styles

44

Qie, Shuyan, Yuanyuan Ran, Xiaosheng Lu, Wei Su, Wei Li, Jianing Xi, Weijun Gong, and Zongjian Liu. "Candesartan modulates microglia activation and polarization via NF-κB signaling pathway." International Journal of Immunopathology and Pharmacology 34 (January 2020): 205873842097490. http://dx.doi.org/10.1177/2058738420974900.

Full text

Abstract:

Microglia are diverse cells that acquire different functional phenotypes in response to microenvironment in which they reside. Several transcriptional regulators have been identified that regulate different microglia phenotypes. They are mainly stimulated into two opposing phenotypes, classically (M1) and alternatively (M2) phenotype. Regulating microglia polarization from M1 to M2 state has been suggested as a potential therapeutic approach in treatment of CNS disorders. Candesartan, an angiotensin II type I receptors antagonist, exerts beneficial effects for antioxidant, anti-inflammation, neurotrophic, and anti-apoptotic function. However, the effect of candesartan on microglia polarization and underlying mechanisms remain unknown. In this study, the resting microglia were stimulated to M1 microglia with lipopolysaccharide (LPS) and interferon-γ (IFN-γ), and then treated with vehicle or candesartan for 24 h. RT-PCR was utilized to detect the mRNA expression of microglia phenotype markers and inflammatory cytokines. Microglia phenotype markers and toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) pathway were determined by western blot. A neuron-microglia co-culture system was used to determine whether candesartan could ameliorate the neurotoxic effect of M1 microglia to oxygen-glucose deprivation (OGD) neuron. Candesartan treatment reduced the expression of M1 markers, and increased M2 markers. Meanwhile, candesartan reduced fluorescence intensity and protein level of M1 marker and enhanced M2 marker. Candesartan also regulated the neuroinflammatory response via reducing the release of pro-inflammatory cytokines and increasing anti-inflammatory cytokines in LPS + IFN-γ stimulated BV2 cells. Candesartan markedly inhibited the protein level of TLR4, the phosphorylation of IKBα and p65, and suppressed nuclear translocation of NF-κB p65. BAY 11-7085, a NF-κB inhibitor, remarkably enlarged the inhibitory effect of candesartan on NF-κB pathway. In addition, M1 phenotype microglia exacerbated post-OGD N2a cells death and LDH release, whereas candesartan reversed such neurotoxic effect. Candesartan treatment may ameliorate stroke-induced neuronal damage through shifting microglia to M2 phenotype in a TLR4/NF-κB-dependent manner.

APA, Harvard, Vancouver, ISO, and other styles

45

Xiao, Liang, Luciana Simao do Carmo, Jason D. Foss, Wei Chen, and David G. Harrison. "Sympathetic Enhancement of Memory T-Cell Homing and Hypertension Sensitization." Circulation Research 126, no. 6 (March 13, 2020): 708–21. http://dx.doi.org/10.1161/circresaha.119.314758.

Full text

Abstract:

Rationale: Effector memory T lymphocytes (T EM cells) exacerbate hypertension in response to repeated hypertensive stimuli. These cells reside in the bone marrow for prolonged periods and can be reactivated on reexposure to the hypertensive stimulus. Objective: Because hypertension is associated with increased sympathetic outflow to the bone marrow, we hypothesized that sympathetic nerves regulate accumulation and reactivation of bone marrow–residing hypertension-specific T EM cells. Methods and Results: Using unilateral superior cervical ganglionectomy in wild-type C57BL/6 mice, we showed that sympathetic nerves create a bone marrow environment that supports residence of hypertension-specific CD8 + T cells. These cells, defined by their proliferative response on coculture with dendritic cells from Ang (angiotensin) II–infused mice, were reduced in denervated compared with innervated bone of Ang II–infused mice. Adoptively transferred CD8 + T cells from Ang II–infused mice preferentially homed to innervated compared with denervated bone. In contrast, ovalbumin responsive T cells from OT-I mice did not exhibit this preferential homing. Increasing superior cervical ganglion activity by activating Gq-coupled designer receptor exclusively activated by designer drug augmented CD8 + T EM bone marrow accumulation. Adoptive transfer studies using mice lacking β2AR (β2 adrenergic receptors) indicate that β2AR in the bone marrow niche, rather than T-cell β2AR is critical for T EM cell homing. Inhibition of global sympathetic outflow using Gi-coupled DREADD (designer receptor exclusively activated by designer drug) injected into the rostral ventrolateral medulla or treatment with a β2AR antagonist reduced hypertension-specific CD8 + T EM cells in the bone marrow and reduced the hypertensive response to a subsequent response to low dose Ang II. Conclusions: Sympathetic nerves contribute to the homing and survival of hypertension-specific T EM cells in the bone marrow after they are formed in hypertension. Inhibition of sympathetic nerve activity and β2AR blockade reduces these cells and prevents the blood pressure elevation and renal inflammation on reexposure to hypertension stimuli.

APA, Harvard, Vancouver, ISO, and other styles

46

Lai, Yanxian, Jianyong Li, Lintao Zhong, Xiang He, Xiaoyun Si, Yili Sun, Yanmei Chen, et al. "The pseudogene PTENP1 regulates smooth muscle cells as a competing endogenous RNA." Clinical Science 133, no. 13 (July 2019): 1439–55. http://dx.doi.org/10.1042/cs20190156.

Full text

Abstract:

AbstractThe long non-coding RNA (lncRNA) PTENP1 is a pseudogene of phosphatase and tensin homologue deleted on chromosome ten (PTEN), has been implicated in smooth muscle cell (SMC) proliferation and apoptosis. PTENP1 is the pseudogene of PTEN. However, it is unclear whether and how PTENP1 functions in the proliferation and apoptosis of human aortic SMCs (HASMCs). Here, we hypothesised that PTENP1 inhibits HASMC proliferation and enhances apoptosis by promoting PTEN expression. PCR analysis and Western blot assays respectively showed that both PTENP1 and PTEN were up-regulated in human aortic dissection (AD) samples. PTENP1 overexpression significantly increased the protein expression of PTEN, promoted apoptosis and inhibited the proliferation of HASMCs. PTENP1 silencing exhibited the opposite effects and mitigated H2O2-induced apoptosis of HASMCs. In an angiotensin II (Ang II)-induced mouse aortic aneurysm (AA) model, PTENP1 overexpression potentiated aortic SMC apoptosis, exacerbated aneurysm formation. Mechanistically, RNA pull-down assay and a series of luciferase reporter assays using miR-21 mimics or inhibitors identified PTENP1 as a molecular sponge for miR-21 to endogenously compete for the binding between miR-21 and the PTEN transcript, releasing PTEN expression. This finding was further supported by in vitro immunofluorescent evidence showing decreased cell apoptosis upon miR-21 mimic administration under baseline PTENP1 overexpression. Ex vivo rescue of PTEN significantly mitigated the SMC apoptosis induced by PTENP1 overexpression. Finally, Western blot assays showed substantially reduced Akt phosphorylation and cyclin D1 and cyclin E levels with up-regulated PTENP1 in HASMCs. Our study identified PTENP1 as a mediator of HASMC homeostasis and suggests that PTENP1 is a potential target in AD or AA intervention.

APA, Harvard, Vancouver, ISO, and other styles

47

Venketasubramanian, Narayanaswamy, Craig Anderson, Hakan Ay, Selma Aybek, Waleed Brinjikji, Gabriel R. de Freitas, Oscar H. Del Brutto, et al. "Stroke Care during the COVID-19 Pandemic: International Expert Panel Review." Cerebrovascular Diseases 50, no. 3 (2021): 245–61. http://dx.doi.org/10.1159/000514155.

Full text

Abstract:

Background: Coronavirus disease 2019 (COVID-19) has placed a tremendous strain on healthcare services. This study, prepared by a large international panel of stroke experts, assesses the rapidly growing research and personal experience with COVID-19 stroke and offers recommendations for stroke management in this challenging new setting: modifications needed for prehospital emergency rescue and hyperacute care; inpatient intensive or stroke units; posthospitalization rehabilitation; follow-up including at-risk family and community; and multispecialty departmental developments in the allied professions. Summary: The severe acute respiratory syndrome coronavirus 2 uses spike proteins binding to tissue angiotensin-converting enzyme (ACE)-2 receptors, most often through the respiratory system by virus inhalation and thence to other susceptible organ systems, leading to COVID-19. Clinicians facing the many etiologies for stroke have been sobered by the unusual incidence of combined etiologies and presentations, prominent among them are vasculitis, cardiomyopathy, hypercoagulable state, and endothelial dysfunction. International standards of acute stroke management remain in force, but COVID-19 adds the burdens of personal protections for the patient, rescue, and hospital staff and for some even into the postdischarge phase. For pending COVID-19 determination and also for those shown to be COVID-19 affected, strict infection control is needed at all times to reduce spread of infection and to protect healthcare staff, using the wealth of well-described methods. For COVID-19 patients with stroke, thrombolysis and thrombectomy should be continued, and the usual early management of hypertension applies, save that recent work suggests continuing ACE inhibitors and ARBs. Prothrombotic states, some acute and severe, encourage prophylactic LMWH unless bleeding risk is high. COVID-19-related cardiomyopathy adds risk of cardioembolic stroke, where heparin or warfarin may be preferable, with experience accumulating with DOACs. As ever, arteritis can prove a difficult diagnosis, especially if not obvious on the acute angiogram done for clot extraction. This field is under rapid development and may generate management recommendations which are as yet unsettled, even undiscovered. Beyond the acute management phase, COVID-19-related stroke also forces rehabilitation services to use protective precautions. As with all stroke patients, health workers should be aware of symptoms of depression, anxiety, insomnia, and/or distress developing in their patients and caregivers. Postdischarge outpatient care currently includes continued secondary prevention measures. Although hoping a COVID-19 stroke patient can be considered cured of the virus, those concerned for contact safety can take comfort in the increasing use of telemedicine, which is itself a growing source of patient-physician contacts. Many online resources are available to patients and physicians. Like prior challenges, stroke care teams will also overcome this one. Key Messages: Evidence-based stroke management should continue to be provided throughout the patient care journey, while strict infection control measures are enforced.

APA, Harvard, Vancouver, ISO, and other styles

48

Kwiatkowski, Boguslaw A., ZhaoMing Dong, and Robert E. Richard. "The Identification of Genes Cooperating with Mpl Signaling Using Insertional Mutagenesis." Blood 112, no. 11 (November 16, 2008): 3860. http://dx.doi.org/10.1182/blood.v112.11.3860.3860.

Full text

Abstract:

Abstract In addition to its role in megakaryopoiesis and platelet production, thrombopoietin activation of its receptor, myeloproliferative leukemia virus protooncogene (Mpl), results in hematopoietic stem cell (HSC) homeostasis and self-renewal. Mutations in the Mpl gene have been shown to be associated with myeloproliferative disorders. In an attempt to identify genes that could cooperate with Mpl signaling leading to an increase in cell survival and proliferation, we have used retroviral expression of a drug dependent, dimerizable, fusion protein which contains the cytoplasmic domain of Mpl. In previous experiments the expression of this protein in both mouse and human blood progenitors resulted in drug dependent hematopoietic cell expansion. We cloned a bacterial shuttle plasmid carrying the Neo gene and a bacterial origin of replication into the 3′ untranslated region of the well-described MSCV based retroviral vector MGIFM to produce the MGIFMNO vector. The shuttle plasmid allows nonbiased recovery of provirus genomic integration sites. This vector can interrupt gene structure through insertion, and has an intact long terminal repeat which can activate adjacent genes. We transduced the human leukemia cell line K562 with the MGIFMNO vector carrying inducible Mpl fusion construct and bacterial shuttle plasmid. The transduction efficiency and relative Mpl expression were assayed by GFP expression since GFP and the Mpl fusion gene are co-expressed through an internal ribosome entry site (IRES). After transduction, the endogenous, transforming Bcr-Abl kinase was blocked using imatinib, and cells dependent on Mpl signaling were selected by the addition of the dimerizer drug, AP20187. In the absence of Mpl signaling the cells underwent erythroid differentiation and died. A small proportion of the transduced cells (3%) survived in the presence of AP20187. The mean fluorescent intensity of the surviving cells was increased relative to non-selected, transduced cells indicating that selection required a high level of Mpl expression. The surviving cells in long term culture were dependent on Mpl signaling and were sensitive to a Jak2 inhibitor, AG490. We cloned retroviral integration sites from the established Mpl dependent population using the plasmid rescue method. A scoring system to assign relevance to isolated integration sites was developed, based on: multiple independent recoveries, relative distance from a target gene, and proximity to a target gene that encodes a product involved in cell cycle, apoptosis, senescence, or gene expression regulation. Cells that have a proliferative advantage and are dependent on Mpl signaling should contain synergistic mutations. Insertion sites in genomic regions appearing repeatedly in multiple experiments are considered highly significant. A preliminary screen of 46 positive integration clones revealed 17 independent integration sites, confirming feasibility of the screening method. Within the rescued integrations we identified possible candidate genes including: the RSL1D1 gene, also labeled PBK1 – nucleostemin interacting protein (nucleostemin was suggested to regulate HSC proliferation), the acidic nuclear phosphoprotein 32 family member B – cell cycle and survival factor, the SH3-domain kinase binding protein 1 – Cbl interacting protein (Cbl was indicated in a repression of HSC self renewal), and Angiotensin II receptor-associated protein isoform E. Large scale screening of integration sites and experimental analysis of candidate genes are under way.

APA, Harvard, Vancouver, ISO, and other styles

49

Olry de Labry Lima, Antonio, Óscar Díaz Castro, Jorge M. Romero-Requena, M. de los Reyes García Díaz-Guerra, Virginia Arroyo Pineda, M. Belén de la Hija Díaz, Meritxell Ascanio, Josep Darbà, and Josep M. Cruzado. "Hyperkalaemia management and related costs in chronic kidney disease patients with comorbidities in Spain." Clinical Kidney Journal, April 7, 2021. http://dx.doi.org/10.1093/ckj/sfab076.

Full text

Abstract:

Abstract Background Hyperkalaemia (HK) is a common electrolyte disorder in patients with chronic kidney disease (CKD) and/or treated with renin–angiotensin–aldosterone system inhibitors (RAASis). The aim of this study is to determine the severity, current management and cost of chronic HK. Methods We performed a retrospective cohort study of patients with chronic HK and CKD, heart failure or diabetes mellitus between 2011 and 2018. The study follow-up was 36 months. Results A total of 1499 patients with chronic HK were analysed: 66.2% presented with mild HK, 23.4% with moderate HK and 10.4% with severe HK. The severity was associated with CKD stage. Most patients (70.4%) were on RAASi therapies, which were frequently discontinued (discontinuation rate was 39.8, 49.8 and 51.8% in mild, moderate and severe HK, respectively). This RAASi discontinuation was similar with or without resin prescription. Overall, ion-exchange resins were prescribed to 42.5% of patients with HK and prescriptions were related to the severity of HK, being 90% for severe HK. Adherence to resin treatment was very low (36.8% in the first year and 17.5% in the third year) and potassium remained elevated in most patients with severe HK. The annual healthcare cost per patient with HK was €5929, reaching €12 705 in severe HK. Costs related to HK represent 31.9% of the annual cost per HK patient and 58.8% of the specialized care cost. Conclusions HK was usually managed by RAASi discontinuation and ion-exchange resin treatment. Most patients with HK were non-adherent to resins and those with severe HK remained with high potassium levels, despite bearing elevated healthcare expenditures.

APA, Harvard, Vancouver, ISO, and other styles

50

Ismail, Umar, Kiran Sidhu, and Shelley Zieroth. "Hyperkalaemia in Heart Failure." Cardiac Failure Review 7 (May 12, 2021). http://dx.doi.org/10.15420/cfr.2020.29.

Full text

Abstract:

Hyperkalaemia has become an increasingly prevalent finding in patients with heart failure (HF), especially with renin–angiotensin–aldosterone system (RAAS) inhibitors and angiotensin–neprilysin inhibitors being the cornerstone of medical therapy. Patients living with HF often have other comorbidities, such as diabetes and chronic kidney disease, which predispose to hyperkalaemia. Until now, we have not had any reliable or tolerable therapies for the treatment of hyperkalaemia to facilitate implementation or achievement of target doses of RAAS inhibition. Patiromer sorbitex calcium and sodium zirconium cyclosilicate are two novel potassium-binding resins that have shown promise in the management of patients predisposed to developing recurrent hyperkalaemia, and their use may allow for further optimisation of guideline directed medical therapy.

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Resine angiotensine'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles