To clarify whether dopaminergic inhibition of aldosterone secretion is physiologically dependent on stimuli from tropic hormones, we attempted to block angiotensin II (AID- and ACTH-mediated increases in the plasma aldosterone concentration (PAC) with dopamine in normal human subjects. The effect of dopamine on metoclopramide-induced aldosterone secretion also was studied. Six normal male subjects in metabolic balance on a 150 meq/ day sodium and 60 meq/day potassium intake received All infusion at 2, 4, and 6 pmol/kg-min, each dose for 30 min, on each of 2 consecutive days. On the first day, the subjects received a vehicle infusion from 60 min before to the end of the All infusion; on the second day, dopamine (4 μ g/kg-min) was substituted for vehicle. All in the presence of vehicle increased PAC from 5.4 ± 1.3 to 19.9 ± 2.9 ng/100 ml; All in the presence of dopamine increased PAC from 4.8 ± 0.5 to 19.5 ± 1.8 ng/100 ml (P = NS). After an interval of 3 weeks on an ad libitum diet, the same protocol was repeated, except that ACTH (5, 10, and 20 U/h) was substituted for AIL ACTH in the presence of vehicle increased PAC from 8.1 ± 2.7 to 27.3 ± 3.1 ng/100 ml; in the presence of dopamine, ACTH increased PAC from 4.7 ± 0.5 to 34.9 ± 6.1 ng/100 ml (P = NS). Metoclopramide increased PAC from 4.5 ± 0.6 to 17.8 ± 2.3 ng/100 ml in the presence of vehicle and from 4.4 ± 0.5 to 7.2 ± 0.7 ng/100 ml in the presence of dopamine (P < 0.01). Dopamine did not decrease basal PAC. Dopamine inhibits increases in aldosterone secretion induced by dopamine antagonist but does not alter All- or ACTH-in-duced steroid secretion. Acutely, dopaminergic inhibition of aldosterone secretion is independent of All and ACTH.