Short Term Effects of Acute Inhibition of the Angiotensin-Converting Enzyme on the Renin-Angiotensin System and Plasma Atrial Natriuretic Peptide in Healthy Dogs fed a Low-Sodium Diet Versus a Normal-Sodium Diet

Abstract. The purpose of the present study was to evaluate the role of the renin-angiotensin system in the secretion of aldosterone during restriction of dietary sodium intake. Rats were kept on control or low-sodium diet for one week. On the 7th morning of diet osmotic minipumps filled with the angiotensin converting enzyme inhibitor (CEI) SQ 20,881, or empty pumps, were implanted subcutaneously (sc). The rats were sacrificed 23 h later. Peripheral blood was analyzed for hormones and electrolytes. Adrenal capsular tissue (z. glomerulosa) was incubated for the determination of the conversion of [3H]corticosterone to [3H]aldosterone. Sodium depletion had no effect on plasma sodium, but it increased potassium concentration. Infusion of CEI had no significant effect on plasma electrolytes. Plasma renin activity was increased both by sodium depletion and CEI. The mean serum aldosterone level was twelve times higher in sodium depleted animals than in controls. Aldosterone level was reduced by about 60 per cent in CEI-infused animals both on control and low-sodium diet. The conversion of corticosterone to aldosterone was significantly stimulated by sodium deprivation. This effect was also inhibited by the CEI SQ 20,881.

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Transcription of (pro)renin mRNA in the rat adrenal cortex, and the effects of ACTH treatment and a low sodium diet

Journal of Endocrinology ◽

10.1677/joe.0.1570217 ◽

1998 ◽

Vol 157 (2) ◽

pp. 217-223 ◽

Cited By ~ 4

Author(s):

MM Ho ◽

GP Vinson

Keyword(s):

Renin Angiotensin System ◽

Zona Fasciculata ◽

Chronic Stimulation ◽

Angiotensin System ◽

Sodium Diet ◽

Adult Rat ◽

Low Sodium Diet ◽

Low Sodium ◽

Renin Mrna

Transcription of the (pro)renin gene in the adult rat adrenal gland was studied by non-isotopic in situ hybridization. In glands from control (untreated) animals, transcription was relatively sparse, and occurred mostly in the outer zona fasciculata. Treatment with ACTH increased the apparent signal in both the glomerulosa and in fasciculata zones. A low sodium diet initially enhanced the transcription signal specifically in the glomerulosa, but as the regime was extended from 5 days to more than 2 weeks, the signal was also increased dramatically in the zona reticularis. The results emphasize the potential importance of the intraglandular renin-angiotensin system, particularly under conditions of chronic stimulation. They also suggest that angiotensin II, as well as being the major regulator of the glomerulosa, may also have some role in inner adrenocortical zone functions.

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Angiotensin augments epinephrine release in pithed rats fed a low-sodium diet

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1990.258.1.r187 ◽

1990 ◽

Vol 258 (1) ◽

pp. R187-R192 ◽

Cited By ~ 1

Author(s):

R. R. Vollmer ◽

S. P. Corey ◽

S. A. Meyers ◽

E. M. Stricker ◽

S. J. Fluharty

Keyword(s):

Angiotensin Ii ◽

Sodium Intake ◽

Renin Angiotensin System ◽

Dietary Sodium ◽

Angiotensin System ◽

Renin Angiotensin ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium ◽

Pithed Rats

In confirmation of previous studies, the amount of epinephrine released into blood during electrical stimulation of the thoracolumbar region of the spinal cord in pithed rats on a low-sodium diet (0.01% sodium by weight of diet for 1 mo) was significantly greater than that observed in rats on a normal sodium diet (0.3% sodium by weight of diet). The present work assessed the extent to which endogenously formed angiotensin II influences this neurally mediated adrenal epinephrine release. The augmented release of epinephrine in rats maintained on the low-sodium diet appeared to depend on circulating angiotensin II because blockade of angiotensin II receptors with saralasin decreased the epinephrine release in these animals but not in rats maintained on the normal diet. Similar results were obtained when the renin-angiotensin system was blocked with the converting-enzyme inhibitor captopril. Adrenal epinephrine content was not affected by the dietary sodium intake; however, the catecholamine synthetic capacity was augmented as indicated by a significant induction of tyrosine hydroxylase. In addition, the adrenal medullary angiotensin II receptor density was significantly elevated in animals on the low-sodium diet. These results demonstrate that endogenous angiotensin II is capable of providing a positive modulatory influence on neurally mediated release of adrenal epinephrine, an effect that may require a chronic activation of the renin-angiotensin system as occurs naturally with restricted dietary sodium intake.

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Endothelial function during stimulation of renin-angiotensin system by low-sodium diet in humans

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2001.280.5.h2248 ◽

2001 ◽

Vol 280 (5) ◽

pp. H2248-H2254 ◽

Cited By ~ 4

Author(s):

Torbjørn Omland ◽

Wendy Johnson ◽

Mary Beth Gordon ◽

Mark A. Creager

Keyword(s):

Renin Angiotensin System ◽

Plasma Renin ◽

Concomitant Treatment ◽

Double Blind ◽

Angiotensin System ◽

Renin Angiotensin ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium ◽

Stimulation Of

We examined whether physiological stimulation of the endogenous renin-angiotensin system results in impaired endothelium-dependent vasodilatation in forearm resistance vessels of healthy subjects and whether this impairment can be prevented by angiotensin II type 1 receptor blockade. A low-sodium diet was administered to 27 volunteers who were randomized to concomitant treatment with losartan (100 mg once daily) or matched placebo in a double-blind fashion. Forearm blood flow was assessed by venous occlusion plethysmography at baseline and after 5 days. Endothelium-dependent and -independent vasodilation was assessed by intra-arterial infusion of methacholine and verapamil, respectively. The low-sodium diet resulted in significantly decreased urine sodium excretion (placebo: 146 ± 64 vs. 10 ± 9 meq/24 h, P < 0.001; losartan: 141 ± 56 vs. 14 ± 14 meq/24 h, P < 0.001) and increased plasma renin activity (placebo: 1.0 ± 0.5 vs. 5.0 ± 2.5 ng · ml−1 · h−1, P < 0.001; losartan: 3.8 ± 7.2 vs. 19.1 ± 11.2 ng · ml−1 · h−1, P = 0.006) in both the losartan and placebo groups. With the baseline study as the reference, the diet intervention was not associated with any significant change in endothelium-dependent vasodilation to methacholine in either the placebo ( P = 0.74) or losartan ( P = 0.40) group. We conclude that short-term physiological stimulation of the renin-angiotensin system does not cause clinically significant endothelial dysfunction. Losartan did not influence endothelium-dependent vasodilation in humans with a stimulated renin-angiotensin system.

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Pathological Role of Angiotensin II in Severe COVID-19

TH Open ◽

10.1055/s-0040-1713678 ◽

2020 ◽

Vol 04 (02) ◽

pp. e138-e144 ◽

Cited By ~ 5

Author(s):

Wolfgang Miesbach

Keyword(s):

Angiotensin Ii ◽

Angiotensin Converting Enzyme ◽

Treatment Options ◽

Renin Angiotensin System ◽

Target Cells ◽

Converting Enzyme ◽

Angiotensin System ◽

Angiotensin Converting Enzyme 2 ◽

Renin Angiotensin ◽

Novel Coronavirus

AbstractThe activated renin–angiotensin system induces a prothrombotic state resulting from the imbalance between coagulation and fibrinolysis. Angiotensin II is the central effector molecule of the activated renin–angiotensin system and is degraded by the angiotensin-converting enzyme 2 to angiotensin (1–7). The novel coronavirus infection (classified as COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as acute respiratory distress syndrome, sepsis, and death in a proportion of patients, mostly elderly patients with preexisting comorbidities. SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptor to enter the target cells, resulting in activation of the renin–angiotensin system. After downregulating the angiotensin-converting enzyme 2, the vasoconstrictor angiotensin II is increasingly produced and its counterregulating molecules angiotensin (1–7) reduced. Angiotensin II increases thrombin formation and impairs fibrinolysis. Elevated levels were strongly associated with viral load and lung injury in patients with severe COVID-19. Therefore, the complex clinical picture of patients with severe complications of COVID-19 is triggered by the various effects of highly expressed angiotensin II on vasculopathy, coagulopathy, and inflammation. Future treatment options should focus on blocking the thrombogenic and inflammatory properties of angiotensin II in COVID-19 patients.

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Resveratrol ameliorates the cyclosporine-induced vascular and renal impairments: possible impact of the modulation of renin–angiotensin system

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2018-0753 ◽

2019 ◽

Vol 97 (12) ◽

pp. 1115-1123 ◽

Cited By ~ 2

Author(s):

Seldag Bekpinar ◽

Ece Karaca ◽

Selin Yamakoğlu ◽

F. İlkay Alp-Yıldırım ◽

Vakur Olgac ◽

...

Keyword(s):

Angiotensin Ii ◽

Angiotensin Converting Enzyme ◽

Renin Angiotensin System ◽

Immunosuppressive Drug ◽

Oxidative Stress Marker ◽

Converting Enzyme ◽

Angiotensin System ◽

Renin Angiotensin ◽

System Components ◽

Renal Tubular

Cyclosporine, an immunosuppressive drug, exhibits a toxic effect on renal and vascular systems. The present study investigated whether resveratrol treatment alleviates renal and vascular injury induced by cyclosporine. Cyclosporine (25 mg/kg per day, s.c.) was given for 7 days to rats either alone or in combination with resveratrol (10 mg/kg per day, i.p.). Relaxation and contraction responses of aorta were examined. Serum levels of blood urea nitrogen, creatinine, angiotensin II, and angiotensin 1-7 were measured. Histopathological examinations as well as immunostaining for 4-hydroxynonenal and nitrotyrosine were performed in the kidney. RNA expressions of renin–angiotensin system components were also measured in renal and aortic tissues. Cyclosporine decreased the endothelium-dependent relaxation and increased vascular contraction in the aorta. It caused renal tubular degeneration and increased immunostaining for 4-hydroxynonenal, an oxidative stress marker. Cyclosporine also caused upregulations of the vasoconstrictive renin–angiotensin system components in renal (angiotensin-converting enzyme) and aortic (angiotensin II type 1 receptor) tissues. Resveratrol co-treatment prevented the cyclosporine-related deteriorations. Moreover, it induced the expressions of vasodilatory effective angiotensin-converting enzyme 2 and angiotensin II type 2 receptor in aorta and kidney, respectively. We conclude that resveratrol may be effective in preventing cyclosporine-induced renal tubular degeneration and vascular dysfunction at least in part by modulating the renin–angiotensin system.

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Polymorphisms of the angiotensin-converting enzyme and angiotensinogen gene in patients with atrial fibrillation

Journal of the Renin-Angiotensin-Aldosterone System ◽

10.1177/1470320311399605 ◽

2011 ◽

Vol 12 (4) ◽

pp. 549-556 ◽

Cited By ~ 7

Author(s):

Nurdan Papila Topal ◽

Beste Ozben ◽

Veysel Sabri Hancer ◽

Azra Meryem Tanrikulu ◽

Reyhan Diz-Kucukkaya ◽

...

Keyword(s):

Atrial Fibrillation ◽

Angiotensin Converting Enzyme ◽

Left Atrium ◽

Renin Angiotensin System ◽

Left Ventricular ◽

Converting Enzyme ◽

Angiotensin System ◽

Ras Genes ◽

Angiotensinogen Gene ◽

M235t Polymorphism

Activation of the renin–angiotensin system (RAS) is associated with atrial fibrillation (AF). The aim of this study was to investigate the relation between AF and polymorphisms in RAS. One hundred and fifty patients with AF, 100 patients with no documented episode of AF and 100 healthy subjects were consecutively recruited into the study. The angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism, and the M235T, A-20C, and G-6A polymorphisms of the angiotensinogen gene were genotyped. Patients with AF had significantly lower frequency of II genotype of ACE I/D and higher frequency of angiotensinogen M235T polymorphism T allele and TT genotype and G-6A polymorphism G allele and GG genotype compared with the controls. AF patients had significantly larger left atrium, higher left ventricular mass index (LVMI) and higher frequency of significant valvular pathology. ACE I/D polymorphism II genotype, angiotensinogen M235T polymorphism TT genotype and G allele and GG genotype of angiotensinogen G-6A polymorphism were still independently associated with AF when adjusted for left atrium, LVMI and presence of significant valvular pathology. Genetic predisposition might be underlying the prevalence of acquired AF. Patients with a specific genetic variation in the RAS genes may be more liable to develop AF.

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