Several studies suggested that dopamine may be one of the inhibitory modulators of aldosterone secretion. Metoclopramide, a selective antagonist for dopamine D-2 receptors, increases both basal plasma aldosterone levels and the aldosterone response to angiotensin II (Ang II) in rats and humans kept on a high sodium intake, these effects being blocked by dopamine infusion. Dopamine, which has no significant effects on Ang II-induced aldosterone secretion in sodium-replete subjects, inhibits the hormonal response to Ang II infusion in sodium-depleted normal subjects, suggesting that the sodium balance state may be an important factor in the dopaminergic mechanisms controlling aldosterone secretion. The effect of dopamine on the hormone production is mediated by D-2 receptors in the adrenal cortex as shown by in vitro studies with isolated adrenal glomerulosa cells. Clinical studies have shown that dihydroergotoxine, a selective D-2 agonist, suppresses the aldosterone secretion induced by sodium depletion in hypertensive patients, an effect blocked by sulpiride. This mechanism could be of relevant therapeutic interest in its contribution to the natriuretic effects of dopaminergic agonists, which have clinical applications in the treatment of hypertension and congestive heart failure.