The effect of angiotensin II infusion on plasma corticosteroid concentrations in normal man

Mason, P A; Fraser, Robert; Morton, J. J.; Semple, P. F.; Wilson, Ana Maria Miranda Martins

doi:10.1016/0022-4731(76)90190-4

Cited by 33 publications

(18 citation statements)

References 18 publications

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“…Infusion into normal subjects, whether sodium replete or deplete, raises the plasma concentrations of aldosterone and 18-hydroxycorticosterone but not those of other corticosteroids (Mason, Fraser, Morton, Semple & Wilson, 1976;Mason, Fraser, Morton, Semple & Wilson, 1977). In isolated zona glomerulosa cells, increases in aldosterone production are accompanied by parallel rises in the production of its precursors (Tait et al, 1974b;Bing & Schulster, 1977).…”

Section: Angiotensinmentioning

confidence: 95%

Control of Aldosterone Secretion

et al. 1979

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Section: Angiotensinmentioning

confidence: 95%

Control of Aldosterone Secretion

et al. 1979

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“…However, the mechanism whereby the addition of mineralocorticoids to hydrocortisone would allow better therapeutic balance even in nonsalt-losing patients is poorly understood. In particular, the role of angiotensin as a physiological regulator of cortisol secretion has not yet been established (4)(5)(6). In this study performed in patients with CAH, the 21-hydroxylase deficiency permitted us to demonstrate the direct action of angiotensin on adrenal steroidogenesis.…”

mentioning

confidence: 95%

Angiotensin and Adrenal Steroidogenesis: Study of 21-Hydroxylase-Deficient Congenital Adrenal Hyperplasia

Schaison

Couzinet

Gourmelen

et al. 1980

The Journal of Clinical Endocrinology & Metabolism

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The effects of angiotensin have been studied in four adult patients with the simple virilizing form of congenital adrenal hyperplasia due to 21-hydroxylase deficiency. They were treated with hydrocortisone (25 mg/day) throughout this investigation. Plasma ACTH was normal in three cases, and androstenedione was normal in all cases. However, urinary pregnanetriol, plasma 17-hydroxyprogesterone (17 OHP), aldosterone, and renin activity was increased. The patients were then submitted to three protocols: sodium depletion (10 meq Na/day) for 5 days, sodium repletion (200 meq Na/day) for 5 days, and angiotensin infusion (sufficient to maintain a pressor response) for 60 min. Urinary pregnanetriol, plasma 17 OHP, and androstenedione levels increased in all patients after sodium depletion and decreased after sodium repletion. Plasma ACTH levels were not modified by changes in the sodium balance. Furthermore, angiotensin infusion increased aldosterone and 17 OHP plasma concentrations without any change in the plasma ACTH level. This study shows the direct action of angiotensin on adrenal steroidogenesis, at least in 21-hydroxylase deficiency. It confirms that even in the simple virilizing form, combined treatment with glucocorticoids and mineralocorticoids helps to normalize plasma 17 OHP levels.

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“…This suggests that circulating renin is needed for the synthesis of angiotensin in the myocardium. Moreover, a role for circulating renin is also suggested by increased aldosterone synthesis in response to intravenous angiotensin II infusions [Ganong et al 1962;Mason et al 1976;Blair-West et al 1962]. In summary, a role for circulating renin seems indisputable and, thus, its inhibition may participate in putative beneficial effects.…”

Section: Direct Renin Inhibition: Extricating Facts From Façadesmentioning

confidence: 99%

Direct renin inhibition: extricating facts from façades

Juncos¹

2013

Therapeutic Advances in Cardiovascular Disease

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Abstract:The renin-angiotensin system (RAS) affects vascular tone, cardiac output and kidney function. By these means the RAS plays a key role in the pathogenesis of arterial hypertension. As a result, RAS inhibition is highly effective not only in lowering blood pressure but also in reducing kidney disease progression (particularly when associated with proteinuria) and cardiovascular events.Among RAS blocking agents, direct renin inhibitors have shown not only excellent efficacy in hypertension control but also pharmacologic tolerance that is comparable with other reninangiotensin suppressors. Indeed, aliskiren, the only direct renin inhibitor available is effective in controlling blood pressure as monotherapy or in combination with other antihypertensive drugs, irrespective of patient's age, ethnicity or sex. It is also effective in patients with metabolic syndrome, obesity and diabetes. Long-term studies comparing 'hard endpoints' of aliskiren therapy versus treatment with other RAS inhibitors, including cardiac and kidney protection, are currently ongoing. Combined with other antihypertensive agents, aliskiren not only improves their hypotensive response but may also lessen the adverse effects of other drugs. In high-risk patients, however, precautions should be taken when combining two or more renin-angiotensin inhibiting agents, as tissue perfusion may be highly renin-dependent in these patients and serious adverse side effects could take place.

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The effect of angiotensin II infusion on plasma corticosteroid concentrations in normal man

Cited by 33 publications

References 18 publications

Control of Aldosterone Secretion

Control of Aldosterone Secretion

Angiotensin and Adrenal Steroidogenesis: Study of 21-Hydroxylase-Deficient Congenital Adrenal Hyperplasia

Direct renin inhibition: extricating facts from façades

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