1991Clinical EndocrinologyRequires access

Role of peripherally infused angiotensin II on the human hypothalamic–pituitary–adrenal axis

Aldo E. Calogero, Marla C. Fornito, Antonia Aiiffl, Enzo Vicarl, Marla L. Moncada, Franco Mantero, P Polosa, Rosario D’Agata

Open publisher page 11 citations

Abstract

Although angiotensin II (AII), a potent vasoconstrictor agent, has been reported to stimulate the hypothalamic-pituitary-adrenal (HPA) axis of laboratory animals, its role in the regulation of this axis in humans appears to be controversial. To examine this question, AII (Val5-AII amide) was infused intravenously into 19 male normal volunteers at the doses of 0, 1, 3.3 and 10 ng/kg/min for 30 min. AII had no effect on plasma ACTH, cortisol, corticotrophin-releasing hormone, arginine vasopressin, and atrial natriuretic factor concentrations, nor did it increase systolic or diastolic arterial blood pressure. On the other hand, AII caused a dose-dependent increase of plasma aldosterone concentrations, suggesting that the doses and the mode of AII infusion were effective. Thus, our data show that peripherally infused AII has no detectable effect on the HPA axis function in humans, at doses capable of stimulating plasma aldosterone secretion, its specific target hormone.

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What this paper is about

Although angiotensin II (AII), a potent vasoconstrictor agent, has been reported to stimulate the hypothalamic-pituitary-adrenal (HPA) axis of laboratory animals, its role in the regulation of this axis in humans appears to be controversial. To examine this question, AII (Val5-AII amide) was infused intravenously into 19 male normal volunteers at the doses of 0, 1, 3.3 and 10 ng/kg/min for 30 min. AII had no effect on plasma ACTH, cortisol, corticotrophin-releasing hormone, arginine vasopressin, and atrial natriuretic factor concentrations, nor did it increase systolic or diastolic arterial blood pressure. On the other hand, AII caused a dose-dependent increase of plasma aldosterone concentrations, suggesting that the doses and the mode of AII infusion were effective. Thus, our data show that peripherally infused AII has no detectable effect on the HPA axis function in humans, at doses capable of stimulating plasma aldosterone secretion, its specific target hormone.

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Available abstract

Although angiotensin II (AII), a potent vasoconstrictor agent, has been reported to stimulate the hypothalamic-pituitary-adrenal (HPA) axis of laboratory animals, its role in the regulation of this axis in humans appears to be controversial. To examine this question, AII (Val5-AII amide) was infused intravenously into 19 male normal volunteers at the doses of 0, 1, 3.3 and 10 ng/kg/min for 30 min. AII had no effect on plasma ACTH, cortisol, corticotrophin-releasing hormone, arginine vasopressin, and atrial natriuretic factor concentrations, nor did it increase systolic or diastolic arterial blood pressure. On the other hand, AII caused a dose-dependent increase of plasma aldosterone concentrations, suggesting that the doses and the mode of AII infusion were effective. Thus, our data show that peripherally infused AII has no detectable effect on the HPA axis function in humans, at doses capable of stimulating plasma aldosterone secretion, its specific target hormone.

Key concepts: Internal medicine, Endocrinology, Vasopressin, Aldosterone, Angiotensin II, Blood pressure, Hormone, Renin–angiotensin system

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