Normal cortical bone mass in patients after long term coumadin therapy

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.