Atrial natriuretic peptide inhibits the aldosterone response to angiotensin II in man

Author:

Anderson J. V.1,Struthers A. D.2,Payne N. N.3,Slater J. D. H.3,Bloom S. R.1

Affiliation:

1. Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London

2. Department of Clinical Pharmacology, Royal Postgraduate Medical School, Hammersmith Hospital, London

3. Department of Cobbold Laboratories, Middlesex Hospital, London

Abstract

1. We have investigated the interaction between the recently discovered natriuretic factor alpha human atrial natriuretic peptide (alpha h-ANP) and the renin-angiotensin-aldosterone system in man. 2. Angiotensin II infused with placebo produced a significant rise of plasma aldosterone concentration (mean ± sem increment 352 ± 23 pmol/l, n = 7, P < 0.001). The infusion of alpha h-ANP together with angiotensin II largely abolished the aldosterone response (P < 0.001). 3. Diastolic blood pressure rose in response to the infusion of angiotensin II with placebo (mean increment 21.0 ± 0.9 mmHg, P < 0.001). Systolic blood pressure increased to a lesser degree (mean increment 12.5 ± 0.7 mmHg, P < 0.001). 4. The infusion of alpha h-ANP together with angiotensin II significantly blunted the diastolic pressor response (P < 0.01). This ability of alpha h-ANP to blunt the pressor effect of angiotensin II may be important in the control of systemic blood pressure. 5. The inhibition of angiotensin II-stimulated aldosterone release demonstrates that alpha h-ANP may not only be a circulating natriuretic factor in its own right but that it may also act as a modulator of a related endocrine system.

Publisher

Portland Press Ltd.

Subject

General Medicine

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