Dopaminergic modulation of aldosterone secretion: effect of sodium balance and postural changes.
The influence of an increased endogenous production of angiotensin II and of sodium homeostasis upon the response of plasma aldosterone to metoclopramide administration has been investigated in 5 normal volunteers. Our results show that the increase of plasma aldosterone after metoclopramide administration is independent of angiotensin II, ACTH and potassium, and that it increases even further due to the endogenous production of angiotensin II induced by postural changes. The state of sodium balance seems to influence the response of plasma aldosterone to metoclopramide administration as it occurs with other stimuli of aldosterone secretion.
D000324:Adrenocorticotropic Hormone / Q000502:physiology; D000328:Adult; D000450:Aldosterone / Q000097:blood / Q000378:metabolism*; D004039:Diet, Sodium-Restricted; D004298:Dopamine / Q000502:physiology*; D018492:Dopamine Antagonists; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D008787:Metoclopramide / Q000494:pharmacology*; D011187:Posture; D011188:Potassium / Q000097:blood; D011388:Prolactin / Q000097:blood; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism*
D018492:Dopamine Antagonists; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D012964:Sodium; D012083:Renin; D008787:Metoclopramide; D011188:Potassium; D004298:Dopamine; D006854:Hydrocortisone