Mineralocorticoid and prolactin response to the dopamine antagonist metoclopramide in patients with primary aldosteronism.

Plasma mineralocorticoid and prolactin levels were evaluated before and 15, 30, 60 and 120 min after the administration of 10 mg metoclopramide in seven normotensive volunteers (42 +/- 5 (SD) years), as well as in ten patients with primary aldosteronism five with aldosterone-producing adenoma (49 +/- 4), and five with bilateral hyperplasia (47 +/- 3). Significant increases of plasma aldosterone, 18-hydroxycorticosterone (18-OH-B), and prolactin levels were observed in all normal subjects and in patients with primary aldosteronism after metoclopramide, whereas plasma 18-corticosterone, corticosterone, and cortisol levels as well as plasma renin activity did not change. The absolute increases of plasma aldosterone and 18-OH-B levels after metoclopramide were considerably higher in eight of the ten patients with primary aldosteronism. Furthermore, in patients with hyperplasia the maximum increase of aldosterone and 18-OH-B was delayed, as was the subsequent decrease of plasma aldosterone. Basal prolactin levels were within the normal range in all patients with primary aldosteronism, but the increase of prolactin observed 15 and 30 min after metoclopramide, was elevated in three patients with hyperplasia and in four patients with adenoma. For patients with primary aldosteronism, a positive correlation was found when the absolute maximum increase of plasma aldosterone levels after metoclopramide was plotted against the increase of prolactin (y = 1.11x - 101, r = 0.74, P less than 0.05). Our results suggest that prolactin, aldosterone, and 18-OH-B secretion is under increased inhibitory dopaminergic control in most of the patients with primary aldosteronism. The positive correlation between the metoclopramide-induced increase of plasma aldosterone and prolactin may indicate a common inhibitory dopaminergic mechanism, working on the pituitary and adrenal level.