Dopaminergic modulation of aldosterone responsiveness to angiotensin II with changes in sodium intake

The aldosterone response to infused angiotensin II (AII) is blunted by sodium (Na) loading. Since dopamine levels increase on a high Na diet and dopamine can inhibit aldosterone secretion, it is possible that dopamine mediates the blunted aldosterone secretion in this setting. To test this hypothesis, we assessed whether the dopamine antagonist, metoclopramide (MCP) would enhance the aldosterone response to infused AII. Six normal subjects received graded infusions of AII when they were in metabolic balance on diets containing both 10 and 200 meq Na/day (control infusions). The infusions were then repeated (on the same diets) during the administration of MCP (0.1 mg/kg iv bolus, then 0.05 mg/kg . h). During the control AII infusions, the aldosterone response to the highest dose of AII was significantly less on the 200 meq Na intake than on 10 meq (plasma aldosterone levels increased 17 +/- 5 vs. 30 +/- 8 ng/dl respectively; P less than 0.01). However, MCP administration eliminated this difference in aldosterone responsiveness by significantly enhancing (P less than 0.02) the response to infused AII during the 200 meq Na intake (plasma aldosterone increment of 25 +/- 9 ng/dl). This effect of MCP was limited to the adrenal response to AII: on a given Na intake, the mean blood pressure response to AII was similar both with and without concomitant MCP. These results suggest that dopamine may be an important regulator of the alterations in aldosterone responsiveness to AII that occur during changes in dietary sodium intake.