Dopamine affects angiotensin II-induced steroidogenesis by altering clearance of the peptide in man

Abstract

ABSTRACT Infusion of dopamine is reported to reduce the response of aldosterone to infused angiotensin II in sodium-deplete but not sodium-replete man. Six normal male subjects were infused with angiotensin II in graded doses (2, 4 and 8 ng/kg per min) with or without dopamine (1·0 μg/kg per min) during both dietary sodium repletion and depletion. The responses of both aldosterone and 18-hydroxycorticosterone to infusion of angiotensin II appeared to be reduced by dopamine in sodium-deplete, but not sodium-replete, subjects. However, when the relationships between plasma concentrations of angiotensin II and corticosteroid were examined it was evident that plasma concentrations of angiotensin II were lower when dopamine was infused concurrently with the peptide (P<0·05). In a second study, six sodium-deplete males were infused with angiotensin II at a constant rate (6 ng/kg per min) while dopamine (or placebo) was given in graded doses (0·5,1 and 5 μg/kg per min). Renal plasma flow was estimated from total body clearance of para-aminohippuric acid. Overall, angiotensin II concentrations were lower during dopamine infusion compared with those during infusion of placebo (63·2 ± 9·7 (s.e.m.) vs 92·3±6·4 pmol/l; P<0·01) and this was associated with a 40% increase in effective renal plasma flow (627 ± 68 vs 451 ± 15 ml/min; P < 0·05); there again appeared to be a reduced aldosterone response during combined angiotensin II/dopamine infusion compared with that during infusion of angiotensin II alone (1003 ± 404 vs 1225± 146 pmol/l; 0·05<P<0·1). Dopamine appeared to increase the metabolic clearance of infused angiotensin II, possibly by altering blood flow through vascular beds, such as renal, which degrade the peptide. This may partly explain the effects of dopamine on the response of the adrenal to infusion of angiotensin II in sodium-deplete man; the physiological role of dopamine in the regulation of corticosteroidogenesis remains speculative. J. Endocr. (1987) 113, 139–146