scholarly journals Interruption of the renin-angiotensin system in hypertensive patients by captopril induces sustained reduction in aldosterone secretion, potassium retention and natruiresis.

Hypertension ◽  
1979 ◽  
Vol 1 (3) ◽  
pp. 274-280 ◽  
Author(s):  
S A Atlas ◽  
D B Case ◽  
J E Sealey ◽  
J H Laragh ◽  
D N McKinstry
Keyword(s):  
Renin Angiotensin System ◽  
Aldosterone Secretion ◽  
Angiotensin System ◽  
Hypertensive Patients ◽  
Renin Angiotensin ◽  
Sustained Reduction ◽  
Potassium Retention

Effect of digoxin on the in vitro secretion of renin and angiotensin II/III immunoreactivity by the human adrenal gland

1992 ◽  
Vol 127 (3) ◽  
pp. 210-214 ◽  
Author(s):  
Matteo Pistorello ◽  
Margherita Cimolato ◽  
Francesco Pedini ◽  
Donatella Piovan ◽  
Marco Boscaro ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Renin Angiotensin System ◽  
Aldosterone Secretion ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Superfusion System ◽  
Sustained Reduction ◽  
High Doses

Cardiac glycosides in man inhibit renin secretion, probably through a direct effect at the renal level (i.e. inhibition of juxtaglomerular cell Na/K ATPase). Since there is evidence that the human adrenal possesses an intrinsic renin-angiotensin system, we investigated the effect of digoxin on the in vitro generation of renin and angiotensin II/III, as well as of aldosterone, by the human adrenal gland. Minced normal adrenal tissues were studied in a superfusion system, measuring in the 15-min superfusate fractions active renin by immunoradiometric assay and angiotensin II/III and aldosterone by radioimmunoassay, respectively. In a first set of four experiments using different concentrations of digoxin in sequence for 45 min periods, digoxin 10−5, but not 10−8 and 10−6 mol/l, significantly reduced renin and angiotensin II/III output from adrenals, while no change in aldosterone was observed. In a second set of three experiments, the addition of digoxin 10−5 mol/l for 120 min caused a sustained reduction of renin and angiotensin II/III, but not of aldosterone. In the final experiment, the decrease of renin and angiotensin II/III during superfusion with digoxin 10−5 mol/l was significantly greater than that observed during superfusion with digoxin in the presence of antidigoxin antibodies. Our data indicate that digoxin at high doses reduces renin and angiotensin II/III but not aldosterone secretion by the human adrenal gland. This suggests two different effects of digoxin, probably both mediated by inhibition of the Na/K ATPase activity, on the adrenal renin-angiotensin- and aldosterone-secreting cells.

Renin-angiotensin system and aldosterone secretion during aortic constriction in the rat

1977 ◽  
Vol 232 (5) ◽  
pp. F434-F437 ◽  
Author(s):  
R. H. Freeman ◽  
J. O. Davis ◽  
W. S. Spielman
Keyword(s):  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Bilateral Nephrectomy ◽  
Aortic Constriction ◽  
Aldosterone Secretion ◽  
Experimental Conditions ◽  
Angiotensin System ◽  
Renin Angiotensin

Suprarenal aortic constriction sufficient to reduce renal perfusion pressure by approximately 50% increased aldosterone secretion in anesthetized rats pretreated with dexamethasone. Bilateral nephrectomy under the same experimental conditions blocked the aldosterone response. Additionally, [1-sarcosine, 8-alanine]angiotensin II blocked the response in aldosterone secretion to aortic constriction in dexamethasone-treated rats. Finally, in rats hypophysectomized to exclude the influence of ACTH, the aldosterone response to aortic constriction was blocked by [1-sarcosine, 8-alanine]angiotensin II. The results indicate that angiotensin II increased aldosterone secretion during aortic constriction in the rat. These observations, along with those reported previously in sodium-depleted rats, point to an important overall role for the renin-angiotensin system in the control of aldosterone secretion in the rat.

scholarly journals Acute effects of renin-angiotensin system blockade on arterial function in hypertensive patients

2007 ◽  
Vol 21 (8) ◽  
pp. 654-663 ◽  
Author(s):  
K A Aznaouridis ◽  
K S Stamatelopoulos ◽  
E N Karatzis ◽  
A D Protogerou ◽  
C M Papamichael ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Acute Effects ◽  
Arterial Function ◽  
Angiotensin System ◽  
Hypertensive Patients ◽  
Renin Angiotensin

scholarly journals Impact of Treatment with Renin–Angiotensin System Inhibitors on Clinical Outcomes in Hypertensive Patients Hospitalized with COVID-19

2020 ◽  
Vol 27 (6) ◽  
pp. 561-568 ◽  
Author(s):  
Martin Negreira-Caamaño ◽  
Jesus Piqueras-Flores ◽  
Jorge Martínez-DelRio ◽  
Patricia Nieto-Sandoval-Martin-DeLaSierra ◽  
Daniel Aguila-Gordo ◽  
...  
Keyword(s):  
Clinical Outcomes ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Hypertensive Patients ◽  
Renin Angiotensin

Role of adrenal renin-angiotensin system in the control of aldosterone secretion in sodium-restricted rats

2000 ◽  
Vol 278 (6) ◽  
pp. E1027-E1030 ◽  
Author(s):  
Giuseppina Mazzocchi ◽  
Ludwik K. Malendowicz ◽  
Anna Markowska ◽  
Giovanna Albertin ◽  
Gastone G. Nussdorfer
Keyword(s):  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Zona Glomerulosa ◽  
Normal Diet ◽  
Angiotensin Ii Receptor ◽  
Aldosterone Secretion ◽  
Angiotensin System ◽  
Renin Angiotensin

This study examined the effect of the pharmacological manipulation of adrenal renin-angiotensin system (RAS) on aldosterone secretion from in situ perfused adrenals of rats kept on a normal diet and sodium restricted for 14 days. Neither the angiotensin-converting enzyme inhibitor captopril nor the nonselective angiotensin II receptor antagonist saralasin and the AT1 receptor-selective antagonist losartan affected basal aldosterone output in normally fed rats. In contrast, they concentration dependently decreased aldosterone secretion in sodium-restricted animals, with maximal effective concentration ranging from 10− 7 to 10− 6 M. Captopril (10− 6 M), saralasin (10− 6 M), and losartan (10− 7 M) counteracted aldosterone response to 10 mM K+ in sodium-restricted rats but not in normally fed animals. Collectively, these findings provide evidence that adrenal RAS plays a role in the regulation of aldosterone secretion, but only under conditions of prolonged stimulation of zona glomerulosa probably leading to overexpression of adrenal RAS.

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.

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