Role of angiotensin in sodium appetite of sodium-deplete sheep

1987 ◽  
Vol 253 (3) ◽  
pp. R482-R488 ◽  
Author(s):  
R. S. Weisinger ◽  
D. A. Denton ◽  
R. Di Nicolantonio ◽  
M. J. McKinley ◽  
A. F. Muller ◽  
...  
Keyword(s):  
Intravenous Infusion ◽  
Extracellular Fluid ◽  
Renin Angiotensin System ◽  
Brain Barrier ◽  
Base Line ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood

The role of the renin-angiotensin system (RAS) in the Na appetite of Na-deplete sheep was investigated. Intravenous infusion of the angiotensin-converting enzyme inhibitor, captopril, at 0.01 or 0.1 mg X kg-1 X h-1 did not cause any change in Na intake, although the higher dose caused a marked decrease in mean arterial blood pressure. Intravenous infusion of captopril at 1.0 mg X kg-1 X h-1 over 24 h decreased Na intake by 45-55% in the absence of any change in Na loss. The decrease in Na intake was restored to base-line level or above by concurrent intravenous infusion of angiotensin II (ANG II) at 3.8 or 24 micrograms/h over 24 h but not by intracerebroventricular (ICV) ANG II at 3.8 micrograms/h. In addition, ICV infusion of 0.7 M mannitol (1 ml/h over 3 h), which reduced cerebrospinal fluid (CSF) and brain extracellular fluid [Na], still increased Na intake when combined with intravenous captopril. Water intake was not altered during intravenous captopril or ANG II alone but was increased during ICV ANG II or 0.7 M mannitol (with or without iv captopril). In conclusion, these results suggest that the RAS is involved in the Na appetite of the Na-deplete sheep. Furthermore, it would appear that the brain area involved is one without a blood-brain barrier but with a CSF-brain barrier, such as one of the circumventricular organs. Also, it would appear that the effect of lowered cerebral Na and the effect of activation of the renin-angiotensin system on Na appetite are independent.

scholarly journals Role of renin-angiotensin system in hypotension-evoked thirst: studies with hydralazine

2000 ◽  
Vol 279 (2) ◽  
pp. R576-R585 ◽  
Author(s):  
Sean D. Stocker ◽  
Alan F. Sved ◽  
Edward M. Stricker
Keyword(s):  
Water Intake ◽  
Intravenous Infusion ◽  
Drinking Behavior ◽  
Regression Line ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Systemic Injection ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood

Injection of rats either with diazoxide (25 mg/kg iv), isoproterenol (0.33 mg/kg sc), or hydralazine (HDZ) (10 mg/kg ip) decreased arterial blood pressure from ∼120 to 70–80 mmHg and stimulated renin secretion. However, diazoxide and isoproterenol treatments each stimulated water ingestion, whereas HDZ treatment did not. HDZ treatment did not reduce water intake evoked by systemic injection of hypertonic saline or 20% polyethylene glycol solution or by 24-h water deprivation, suggesting that HDZ treatment did not interfere with drinking behavior. In contrast, HDZ treatment markedly reduced water intake evoked by injection of diazoxide or isoproterenol or by intravenous infusion of renin. Furthermore, a highly significant correlation was observed when plasma ANG II levels were plotted as a function of plasma renin activity after intravenous infusion of renin and after diazoxide and isoproterenol treatments. However, values obtained after HDZ treatment alone or in combination with intravenous infusion of renin did not fall near the 99% confidence interval of the regression line, suggesting that HDZ treatment blocks ANG II production and/or promotes its clearance. Thus rats apparently do not increase water intake after HDZ treatment, because this drug interferes with the renin-angiotensin system. These results provide further evidence that arterial hypotension evokes thirst in rats predominantly by activation of the renin-angiotensin system.

Role of the renin-angiotensin system in drinking of seawater-adapted eels Anguilla japonica: a reevaluation

2000 ◽  
Vol 279 (3) ◽  
pp. R1105-R1111 ◽  
Author(s):  
Yoshio Takei ◽  
Takamasa Tsuchida
Keyword(s):  
Arterial Pressure ◽  
Plasma Osmolality ◽  
Renin Angiotensin System ◽  
Minor Role ◽  
Dependent Manner ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood

The role of ANG II, a potent dipsogenic hormone, in copious drinking of seawater eels was examined. SQ-14225 (SQ), an angiotensin-converting enzyme inhibitor, infused intra-arterially at 0.01–1 μg · kg−1 · min−1, depressed drinking and arterial blood pressure in a dose-dependent manner. The inhibition was accompanied by a small decrease in plasma ANG II concentration, which became significant at 1 μg · kg−1 · min−1. After the infusate was changed back to the vehicle, the depression of drinking and arterial pressure continued for >2 h, although plasma ANG II concentration rebounded above the level before SQ infusion. By contrast, infusion of anti-ANG II serum (0.01–1 μg · kg−1 · min−1) did not suppress drinking and arterial pressure, although plasma ANG II concentration decreased to undetectable levels. Plasma atrial natriuretic peptide and plasma osmolality, which influence drinking rate in eels, did not change during SQ or antiserum infusions. These results suggest that the renin-angiotensin system plays only a minor role in the vigorous drinking observed in seawater eels. The results also suggest that the antidipsogenic and vasodepressor effects of SQ in seawater eels are not due solely to the inhibition of ANG II formation in plasma.

Renal responses to hypoxemia during renin-angiotensin system inhibition in fetal lambs

1985 ◽  
Vol 249 (1) ◽  
pp. R116-R124 ◽  
Author(s):  
K. T. Nakamura ◽  
N. A. Ayres ◽  
R. A. Gomez ◽  
J. E. Robillard
Keyword(s):  
Renin Angiotensin System ◽  
Base Line ◽  
Urinary Flow ◽  
Ang Ii ◽  
Functional Responses ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Renal Hemodynamic ◽  
Excretion Rates

The role of the renin-angiotensin system (RAS) in modulating the renal hemodynamic and functional responses to hypoxemia was studied in chronically catheterized fetal lambs (132-143 days gestation; term 145 days) before and during administration of either captopril or [Sar1-Gly8]ANG II. Base-line mean arterial blood pressure decreased significantly after administration of either captopril or [Sar1-Gly8]ANG II. This decrease was associated with a significant decline in renal vascular resistance (RVR) in captopril-treated fetuses, whereas no changes in RVR were observed in [Sar1-Gly8]ANG II-treated fetuses. However, the decline in renal blood flow (RBF) and the rise in RVR associated with hypoxemia in control fetuses were not attenuated significantly during inhibition of the RAS using either captopril or [Sar1-Gly8]ANG II. Moreover neither captopril nor [Sar1-Gly8]ANG II blunted the hypertensive response associated with fetal hypoxemia. The renal functional response to captopril was different from the response observed during infusion of [Sar1-Gly8]ANG II. Administration of [Sar1-Gly8]ANG II produced significant decreases in urinary flow rate (UFR), glomerular filtration rate (GFR), and urinary electrolyte (Na+, K+, Cl-) excretion rates, whereas no changes were observed during captopril infusion. The effects of hypoxemia on renal function were not modified after captopril. However, [Sar1-Gly8]ANG II tended to increase UFR and GFR, but these changes were pressure-dependent and not directly related to inhibition of the RAS. This study suggests that the RAS is not an important mediator of the fetal renal hemodynamic and functional responses to hypoxemia.

Splanchnic blood flow and hepatic glucose production in exercising humans: role of renin-angiotensin system

2001 ◽  
Vol 281 (6) ◽  
pp. R1854-R1861 ◽  
Author(s):  
Raynald Bergeron ◽  
Michael Kjær ◽  
Lene Simonsen ◽  
Jens Bülow ◽  
Dorthe Skovgaard ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renin Angiotensin System ◽  
Glucose Production ◽  
Splanchnic Blood Flow ◽  
Control Group ◽  
Moderate Exercise ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin

The study examined the implication of the renin-angiotensin system (RAS) in regulation of splanchnic blood flow and glucose production in exercising humans. Subjects cycled for 40 min at 50% maximal O2 consumption (V˙o 2 max) followed by 30 min at 70% V˙o 2 maxeither with [angiotensin-converting enzyme (ACE) blockade] or without (control) administration of the ACE inhibitor enalapril (10 mg iv). Splanchnic blood flow was estimated by indocyanine green, and splanchnic substrate exchange was determined by the arteriohepatic venous difference. Exercise led to an ∼20-fold increase ( P < 0.001) in ANG II levels in the control group (5.4 ± 1.0 to 102.0 ± 25.1 pg/ml), whereas this response was blunted during ACE blockade (8.1 ± 1.2 to 13.2 ± 2.4 pg/ml) and in response to an orthostatic challenge performed postexercise. Apart from lactate and cortisol, which were higher in the ACE-blockade group vs. the control group, hormones, metabolites, V˙o 2, and RER followed the same pattern of changes in ACE-blockade and control groups during exercise. Splanchnic blood flow (at rest: 1.67 ± 0.12, ACE blockade; 1.59 ± 0.18 l/min, control) decreased during moderate exercise (0.78 ± 0.07, ACE blockade; 0.74 ± 0.14 l/min, control), whereas splanchnic glucose production (at rest: 0.50 ± 0.06, ACE blockade; 0.68 ± 0.10 mmol/min, control) increased during moderate exercise (1.97 ± 0.29, ACE blockade; 1.91 ± 0.41 mmol/min, control). Refuting a major role of the RAS for these responses, no differences in the pattern of change of splanchnic blood flow and splanchnic glucose production were observed during ACE blockade compared with controls. This study demonstrates that the normal increase in ANG II levels observed during prolonged exercise in humans does not play a major role in the regulation of splanchnic blood flow and glucose production.

scholarly journals Role of the renin-angiotensin system in the development of severe COVID-19 in hypertensive patients

2020 ◽  
Vol 319 (4) ◽  
pp. L596-L602
Author(s):  
Rodrigo Pacheco Silva-Aguiar ◽  
Diogo Barros Peruchetti ◽  
Patricia Rieken Macedo Rocco ◽  
Alvin H. Schmaier ◽  
Patrícia Machado Rodrigues e Silva ◽  
...  
Keyword(s):  
Critical Role ◽  
Renin Angiotensin System ◽  
Multiple Organ ◽  
Ang Ii ◽  
Angiotensin System ◽  
Hypertensive Patients ◽  
Renin Angiotensin ◽  
Therapeutic Benefits ◽  
Global Threat

A new form of severe acute respiratory syndrome (SARS) caused by SARS-coronavirus 2 (CoV-2), called COVID-19, has become a global threat in 2020. The mortality rate from COVID-19 is high in hypertensive patients, making this association especially dangerous. There appears to be a consensus, despite the lack of experimental data, that angiotensin II (ANG II) is linked to the pathogenesis of COVID-19. This process may occur due to acquired deficiency of angiotensin-converting enzyme 2 (ACE2), resulting in reduced degradation of ANG II. Furthermore, ANG II has a critical role in the genesis and worsening of hypertension. In this context, the idea that there is a surge in the level of ANG II with COVID-19 infection, causing multiple organ injuries in hypertensive patients becomes attractive. However, the role of other components of the renin angiotensin system (RAS) in this scenario requires elucidation. The identification of other RAS components in COVID-19 hypertension may provide both diagnostic and therapeutic benefits. Here, we summarize the pathophysiologic contributions of different components of RAS in hypertension and their possible correlation with poor outcome observed in hypertensive patients with COVID-19.

The role of local and systemic renin angiotensin system activation in a genetic model of sympathetic hyperactivity-induced heart failure in mice

2008 ◽  
Vol 294 (1) ◽  
pp. R26-R32 ◽  
Author(s):  
J. C. B. Ferreira ◽  
A. V. Bacurau ◽  
F. S. Evangelista ◽  
M. A. Coelho ◽  
E. M. Oliveira ◽  
...  
Keyword(s):  
Heart Failure ◽  
Renin Angiotensin System ◽  
Collagen Content ◽  
Ang Ii ◽  
Male Adult ◽  
Angiotensin System ◽  
Sympathetic Hyperactivity ◽  
Renin Angiotensin ◽  
Ras Activation

Sympathetic hyperactivity (SH) and renin angiotensin system (RAS) activation are commonly associated with heart failure (HF), even though the relative contribution of these factors to the cardiac derangement is less understood. The role of SH on RAS components and its consequences for the HF were investigated in mice lacking α2A and α2C adrenoceptor knockout (α2A/α2CARKO) that present SH with evidence of HF by 7 mo of age. Cardiac and systemic RAS components and plasma norepinephrine (PN) levels were evaluated in male adult mice at 3 and 7 mo of age. In addition, cardiac morphometric analysis, collagen content, exercise tolerance, and hemodynamic assessments were made. At 3 mo, α2A/α2CARKO mice showed no signs of HF, while displaying elevated PN, activation of local and systemic RAS components, and increased cardiomyocyte width (16%) compared with wild-type mice (WT). In contrast, at 7 mo, α2A/α2CARKO mice presented clear signs of HF accompanied only by cardiac activation of angiotensinogen and ANG II levels and increased collagen content (twofold). Consistent with this local activation of RAS, 8 wk of ANG II AT1 receptor blocker treatment restored cardiac structure and function comparable to the WT. Collectively, these data provide direct evidence that cardiac RAS activation plays a major role underlying the structural and functional abnormalities associated with a genetic SH-induced HF in mice.

scholarly journals The Prorenin and (Pro)renin Receptor: New Players in the Brain Renin-Angiotensin System?

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Wencheng Li ◽  
Hua Peng ◽  
Dale M. Seth ◽  
Yumei Feng
Keyword(s):  
Renin Angiotensin System ◽  
Ang Ii ◽  
Future Perspectives ◽  
Vasopressin Release ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Treatment Of Hypertension ◽  
High Level ◽  
The Brain

It is well known that the brain renin-angiotensin (RAS) system plays an essential role in the development of hypertension, mainly through the modulation of autonomic activities and vasopressin release. However, how the brain synthesizes angiotensin (Ang) II has been a debate for decades, largely due to the low renin activity. This paper first describes the expression of the vasoconstrictive arm of RAS components in the brain as well as their physiological and pathophysiological significance. It then focus on the (pro)renin receptor (PRR), a newly discovered component of the RAS which has a high level in the brain. We review the role of prorenin and PRR in peripheral organs and emphasize the involvement of brain PRR in the pathogenesis of hypertension. Some future perspectives in PRR research are heighted with respect to novel therapeutic target for the treatment of hypertension and other cardiovascular diseases.

scholarly journals Interactions of Renin-Angiotensin System and COVID-19: The Importance of Daily Rhythms in ACE2, ADAM17 and TMPRSS2 Expression

2021 ◽  
pp. S177-S194
Author(s):  
J ZLACKÁ ◽  
K STEBELOVÁ ◽  
M ZEMAN ◽  
I HERICHOVÁ
Keyword(s):  
Renin Angiotensin System ◽  
Positive Association ◽  
Ang Ii ◽  
Virus Envelope ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Circadian Control ◽  
A Disintegrin And Metalloproteinase

Angiotensin-converting enzyme 2 (ACE2) was identified as a molecule that mediates the cellular entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Several membrane molecules of the host cell must cooperate in this process. While ACE2 serves in a membrane receptor-mediating interaction with the surface spike (S) glycoprotein of SARS-CoV-2 located on the virus envelope, enzyme A disintegrin and metalloproteinase 17 (ADAM17) regulates ACE2 availability on the membrane and transmembrane protease serine 2 (TMPRSS2) facilitates virus-cell membrane fusion. Interestingly, ACE2, ADAM17 and TMPRSS2 show a daily rhythm of expression in at least some mammalian tissue. The circadian system can also modulate COVID-19 progression via circadian control of the immune system (direct, as well as melatonin-mediated) and blood coagulation. Virus/ACE2 interaction causes ACE2 internalization into the cell, which is associated with suppressed activity of ACE2. As a major role of ACE2 is to form vasodilatory angiotensin 1-7 from angiotensin II (Ang II), suppressed ACE2 levels in the lung can contribute to secondary COVID-19 complications caused by up-regulated, pro-inflammatory vasoconstrictor Ang II. This is supported by the positive association of hypertension and negative COVID-19 prognosis although this relationship is dependent on numerous comorbidities. Hypertension treatment with inhibitors of renin-angiotensin system does not negatively influence prognosis of COVID-19 patients. It seems that tissue susceptibility to SARS-CoV-2 shows negative correlation to ACE2 expression. However, in lungs of infected patient, a high ACE2 expression is associated with better outcome, compared to low ACE2 expression. Manipulation of soluble ACE2 levels is a promising COVID-19 therapeutic strategy.

Pivotal role of the renin-angiotensin system in Lyon hypertensive rats

1997 ◽  
Vol 273 (5) ◽  
pp. R1793-R1799 ◽  
Author(s):  
Pierre Lantelme ◽  
Ming Lo ◽  
Laurent Luttenauer ◽  
Jean Sassard
Keyword(s):  
Renin Angiotensin System ◽  
Ace Inhibition ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Adult Age ◽  
Enhanced Sensitivity ◽  
Regional Hemodynamics ◽  
Renal Vascular

We assessed the role of the renin-angiotensin system (RAS) in Lyon genetically hypertensive (LH) and normotensive (LN) rats by measuring 1) kidney renin and prorenin contents; 2) effects of early, prolonged angiotensin-converting enzyme (ACE) inhibition on blood pressure (BP) and regional hemodynamics; and 3) acute and chronic responses to angiotensin II (ANG II) and norepinephrine (NE). At the adult age, LH rats differed from LN rats by elevated BP, left ventricle weight, and vascular resistances, especially in the kidneys, associated with lower kidney renin and prorenin contents. ACE inhibition (perindopril, 3 mg ⋅ kg−1 ⋅ 24 h−1 orally from 3 to 15 wk of age) suppressed the development of hypertension, cardiac hypertrophy, and the increase in renal vascular resistances. No specific hypersensitivity to ANG II could be disclosed in acute conditions. In perindopril-treated LH rats, a 4-wk infusion of ANG II (200 ng ⋅ kg−1 ⋅ min−1) but not of NE (1,000 ng ⋅ kg−1 ⋅ min−1) restored hypertension, mimicked the hemodynamic alterations seen in untreated LH rats, and produced a brief sodium retention. It is concluded that in LH rats, despite a low basal renin secretion, hypertension and hemodynamic abnormalities 1) are fully dependent on an active RAS and 2) may involve an enhanced sensitivity to the chronic effects of ANG II.

Role of the renin-angiotensin system in the systemic microvascular inflammation of alveolar hypoxia

2007 ◽  
Vol 292 (5) ◽  
pp. H2285-H2294 ◽  
Author(s):  
Norberto C. Gonzalez ◽  
Julie Allen ◽  
Eric J. Schmidt ◽  
Alfred J. Casillan ◽  
Teresa Orth ◽  
...  
Keyword(s):  
Ace Inhibitor ◽  
Renin Angiotensin System ◽  
Ace Inhibition ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Alveolar Hypoxia ◽  
Microvascular Inflammation

Alveolar hypoxia (AH) induces widespread systemic inflammation. Previous studies have shown dissociation between microvascular Po2 and inflammation. Furthermore, plasma from AH rats (PAHR) induces mast cell (MC) activation, inflammation, and vasoconstriction in normoxic cremasters, while plasma from normoxic rats does not produce these responses. These results suggest that inflammation of AH is triggered by a blood-carried agent. This study investigated the involvement of the renin-angiotensin system (RAS) in the inflammation of AH. Both an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin II (ANG II) receptor blocker (ANG II RB) inhibited the leukocyte-endothelial adherence produced by AH, as well as the inflammation produced by PAHR in normoxic rat cremasters. MC stabilization with cromolyn blocked the effects of PAHR but not those of topical ANG II on normoxic cremasters, suggesting ANG II generation via MC activation by PAHR. This was supported by the observation that ACE inhibition and ANG II RB blocked the leukocyte-endothelial adherence produced by the MC secretagogue compound 48/80. These results suggest that the intermediary agent contained in PAHR activates MC and stimulates the RAS, leading to inflammation, and imply an RAS role in AH-induced inflammation.

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