Role of prolactin and the renin-angiotensin system in mediating dopaminergic control of aldosterone secretion in the rat.
Blockade of dopaminergic pathways increases aldosterone levels by mechanisms that are not well delineated. Since both prolactin (PRL) and plasma renin activity (PRA) also increase after administration of dopaminergic antagonists, the aldosterone increments may be secondary to these changes. To address these questions, the relationship between plasma aldosterone (PA) and PRL responses to 2 different dopamine receptor antagonists, haloperidol and metoclopramide (MCP) was examined in rats. The PA response to MCP was compared before and after blockade of the renin-angiotensin system with saralasin and after pre-administration of L-dopa. MCP administration produced significant and parallel increments in PA and PRL whereas haloperidol increased PRL without any change in PA or PRA. L-dopa pre-treatment suppressed the early PA response to MCP. Hypophysectomy prior to MCP administration eliminated the PRL response but did not significantly alter the PA response to MCP. Our findings suggest that dopamine has an inhibitory action on the adrenal gland production of aldosterone acting independently of changes in PRL and the renin-angiotensin system.
D000450:Aldosterone / Q000097:blood / Q000378:metabolism*; D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D004298:Dopamine / Q000502:physiology*; D018492:Dopamine Antagonists; D006220:Haloperidol / Q000494:pharmacology; D007016:Hypophysectomy; D007980:Levodopa / Q000494:pharmacology; D008297:Male; D008787:Metoclopramide / Q000494:pharmacology; D011388:Prolactin / Q000502:physiology*; D051381:Rats; D012504:Saralasin / Q000494:pharmacology
D018492:Dopamine Antagonists; D000804:Angiotensin II; D007980:Levodopa; D000450:Aldosterone; D011388:Prolactin; D012504:Saralasin; D006220:Haloperidol; D008787:Metoclopramide; D004298:Dopamine