Lack of direct effect of dopamine on aldosterone secretion in vivo.

Previous work suggests that aldosterone is modulated by dopamine, which exerts an inhibitory effect at the level of the adrenal cortex. This study reports the effect of dopamine on aldosterone secretion in conscious sheep with cervical adrenal transplants in whom endogenous ACTH secretion was suppressed by dexamethasone. In control experiments (n = 7) local adrenal infusions of angiotensin II (AII) (1.6 ng/min for 120 min) increased aldosterone secretion to peak levels (47.8 +/- 6.8 ng/min. mean +/- SEM) at 20 min, after which secretion fell to stable levels (20-28 ng/min) at 60-120 min. On separate days, sheep were restudied (n = 5) during systemic dopamine infusions (4 microgram/kg . min for 90 min), commencing 30 min before AII stimulation. There was no significant difference, either in the pattern or the sensitivity of the aldosterone response to AII, with dopamine infusions. Large intraadrenal infusions of dopamine (10 microgram/min) also failed to alter the aldosterone response to AII. The possibility that aldosterone was already under maximum tonic inhibition by dopamine was studied in four additional experiments using the dopamine blocking drug, metoclopramide. Although the systemic (iv) administration of metoclopramide increased aldosterone in both intact and transplanted sheep, local infusions of metoclopramide (0.5-15 microgram/min intraarterially) had no consistent effect on the aldosterone response to AII, and the addition of dopamine during metoclopramide infusions also had no effect. These results indicate that local (adrenal) dopaminergic mechanisms play little or no part in the regulation of aldosterone secretion in the sheep. The mechanism whereby aldosterone secretion is increased by systemic metoclopramide remains to be explained.