Dopaminergic suppression of angiotensin II-induced aldosterone secretion in man: differential responses during sodium loading and depletion

Previous studies have shown that aldosterone secretion may be inhibited by dopaminergic mechanisms in man. Dopamine does not inhibit aldosterone responses to angiotensin II in sodium-replete normal subjects. Since sodium deficiency is associated with a reduction in renal dopamine formation, we investigated the effect of dopamine on angiotensin II-induced aldosterone secretion in the sodium-depleted state. Six normal subjects in balance at 10 mEq sodium intake (UNaV 17 +/- 2 meq/24 hr) received dopamine 4 micrograms/kg/min or vehicle for 210 minutes on two consecutive days. After 60 minutes of the dopamine or vehicle infusion, the subjects received successive 30-minute infusions of angiotensin II in increasing doses of 0.5, 1, 2, 4 and 6 picomol/kg/min. Control plasma aldosterone concentrations before vehicle or dopamine were 15 +/- 3 (mean 1 +/- SE) and 25 +/- 3 ng/dL, respectively. Aldosterone responses to angiotensin II were greater with vehicle than dopamine at angiotensin II doses of 4 and 6 picomol/kg/min (P less than 0.025). The slope of angiotensin-aldosterone dose-response curve was steeper with vehicle (0.33) than with dopamine (0.16), P less than 0.01. Serum prolactin concentrations were lower with dopamine (1.6 +/- 0.8 ng/mL) than with vehicle (6.4 +/- 1.2 ng/mL, P less than 0.05) by 120 minutes of infusion and remained suppressed with dopamine for the remainder of the dopamine infusion. Diastolic blood pressure was higher (P less than 0.05) with vehicle than with dopamine at angiotensin II doses of 2, 4, and 6 picomol/kg/min. Dopamine administration was associated with an increase in plasma cortisol concentration from 90 to 150 minutes of infusion (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)