Dopaminergic blockade of the renin-angiotensin-aldosterone system: effect of high and low sodium intakes.
Recent investigations suggest that dopamine inhibits aldosterone secretion. To test the hypothesis that dopamine contributes to the reduced aldosterone secretion on a high sodium intake, eight normal subjects were studied in metabolic balance on both 200 and 10 mmol sodium diets. On each diet, the subjects received a constant 4 h intravenous infusion of the dopamine antagonist, metoclopramide (MCP). Although MCP significantly increased plasma aldosterone (PA) throughout the infusion on both diets, the maximum increment in PA was greater on the low (37 +/- 5 ng/dl) than on the high (14 +/- 4 ng/dl) sodium intake (P less than 0.02). The greater response on the low sodium intake could not be ascribed to changes in potassium, cortisol or ACTH. However, plasma renin activity (PRA) and angiotensin II (AII) levels were significantly (P less than 0.01) increased by MCP while on the low but not the high sodium intake. We conclude that the rise in PA while on a high sodium intake reflects dopaminergic antagonism by MCP directly at the level of the adrenal gland. On the low sodium intake, the enhanced PA response to MCP probably reflects both a direct adrenal effect and an indirect effect mediated via activation of the renin-angiotensin system.
D000328:Adult; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D004039:Diet, Sodium-Restricted; D004298:Dopamine / Q000378:metabolism; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D008787:Metoclopramide / Q000494:pharmacology*; D011388:Prolactin / Q000097:blood; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000187:drug effects*; D012964:Sodium / Q000494:pharmacology*
D000804:Angiotensin II; D000450:Aldosterone; D011388:Prolactin; D012964:Sodium; D012083:Renin; D008787:Metoclopramide; D004298:Dopamine; D006854:Hydrocortisone