Dopamine modulates sodium-dependent aldosterone responses to angiotensin II in humans.

Studies have shown that dopamine inhibits angiotensin II (AII)-induced aldosterone secretion in bovine adrenal cells in vitro, but does not alter aldosterone responses to AII in sodium-replete normal humans. We investigated six normal men with plasma cortisol concentrations less than 2 micrograms/dl during oral administration of dexamethasone 0.5 mg every 6 hours for 2 days and in balance at 10 mEq sodium/day intake (UNa V 22 +/- 5 mEq/24 hr). The subjects received either dopamine 4 micrograms/kg/min or vehicle intravenously (i.v.) for 270 minutes on 2 consecutive days. After 120 minutes of dopamine infusion, AII was given in cumulative doses of 0.5, 1, 2, 4, and 6 pmol/kg/min i.v., each dose for 30 minutes. Control plasma aldosterone concentrations before vehicle or dopamine were 12 +/- 2 (mean +/- 1 SE) and 15 +/- 3 ng/dl, respectively. Aldosterone responses to AII were greater with vehicle than dopamine at AII doses of 4 and 6 pmol/kg/min (p less than 0.02). The slope of the AII-aldosterone dose-response curve was steeper with vehicle (0.36) than with dopamine (0.13), p less than 0.0001. Plasma renin activity and serum potassium concentrations were similar with vehicle and dopamine. Dopamine inhibits AII-induced aldosterone secretion during sodium deficiency in humans.