Sodium loading reduces aldosterone responses to angiotensin II (AII) when compared to the sodium restricted state. Recent investigations suggest that dopamine inhibits the aldosterone secretion and may contribute to the alteration in aldosterone response to AII with sodium intake, since administration of the dopamine antagonist, metoclopramide, enhances the aldosterone responses to AII on a high but not a low salt diet. Nonmodulating hypertension is characterized, in part, by a decreased aldosterone response to AII, raising the possibility that an increased dopaminergic inhibition of aldosterone secretion underlies the adrenal defect in nonmodulating hypertension. To assess this possibility, 69 patients with hypertension were characterized in relationship to their modulation status on a low sodium intake. Dopamine levels were significantly higher (P less than .05) in nonmodulators. To assess the physiologic relevance of these findings, the aldosterone response to AII infusion was assessed before and during administration of the dopamine antagonist, metoclopramide, in 13 patients. The adrenal response to AII did not change after metoclopramide in either hypertensive subgroup. Thus, it is unlikely that the adrenal defect is due to the increase in dopamine levels observed in nonmodulators. In the next study, the impact of dietary sodium intake on urinary dopamine levels was compared in normotensive and hypertensive subjects characterized as modulators and nonmodulators. Both modulators and normotensive subjects demonstrated an increase in urinary dopamine excretion in response to a high sodium intake--a feature that was not observed in the nonmodulators. Thus, the sodium retaining tendency of nonmodulators may reflect, at least in part, a reduction in intrarenal dopamine production in response to a sodium load.