Altering angiotensin levels by administration of captopril or indomethacin, or by angiotensin infusion, contributes to an understanding of atrial natriuretic peptide regulation in man.

Abstract

1. Plasma atrial natriuretic peptide (ANP) levels were positively correlated with plasma renin activity (PRA) levels, when blood volume and blood pressure (BP) were not raised in normal subjects (NLS) or patients with postoperative aldosterone-producing adenoma (APA), Bartter's syndrome (BS), Addison's disease, anorexia nervosa, diuretic abuse or salt-losing congenital adrenal hyperplasia. 2. Angiotensin II infusion raised ANP levels in NLS, and patients with BS, pre- and postoperative APA, only when BP rose, suggesting that this effect might be mediated by the rise in BP. 3. Captopril lowered aldosterone and ANP levels in renal artery stenosis, but falling BP levels could mediate this effect. Captopril lowered aldosterone and BP in BS, but did not lower ANP, perhaps because angiotensin remained elevated. 4. Indomethacin lowered ANP when PRA was initially normal or raised (NLS and BS), but not when PRA was suppressed (APA). This effect could not be mediated by BP, which rose, but could be mediated by renin-angiotensin, which fell. 5. Factors other than central blood volume and atrial stretch may modulate ANP levels. Plasma angiotensin II may be such a factor, and may exert an important influence at high levels, especially when blood volume is low.