Stimulation of aldosterone secretion by metoclopramide in humans: apparent independence of renal and pituitary mediation.
Metoclopramide (MP), a dopamine antagonist, stimulates secretion of aldosterone by a mechanism which has not been defined. We examined a potential role for either the kidney or the pituitary to mediate MPs effect on aldosterone secretion. Responses to MP administered i.v. were measured in six anephric and six hypopituitary patients as well as in six normal subjects. MP increased the plasma aldosterone concentration (PAC) in normal subjects in a fashion similar to what had previously been reported. MP produced no increase in plasma levels of renin activity (PRA), cortisol, potassium, or sodium. Three of six anephric patients (all of whom had undetectable PRA) responded to MP with increases in PAC; the magnitude of these responses correlated with the plasma potassium concentration. All six hypopituitary patients showed increases in PAC after MP administration. MP increased plasma prolactin levels in normal subjects and anephric patients; one hypopituitary patient had high basal plasma prolactin levels which increased with MP. In conclusion, neither the kidney nor the pituitary is involved in the mechanism for MP stimulated aldosterone production. These observations suggest that MP may act on the adrenal to evoke secretion of aldosterone.
D000324:Adrenocorticotropic Hormone / Q000502:physiology; D000328:Adult; D000450:Aldosterone / Q000378:metabolism*; D005260:Female; D006801:Humans; D007018:Hypopituitarism / Q000503:physiopathology; D007668:Kidney / Q000502:physiology*; D008297:Male; D008787:Metoclopramide / Q000494:pharmacology*; D010902:Pituitary Gland / Q000502:physiology*; D013268:Stimulation, Chemical
D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D008787:Metoclopramide