Dopaminergic modulation of aldosterone secretion is independent of alterations in renin secretion.
This study was designed to determine if dopaminergic modulation of aldosterone secretion is mediated through the renin-angiotensin system. In rats, intraarterial administration of metoclopramide (MCP), a dopamine antagonist, resulted in a significant elevation of plasma aldosterone (PA) 5 min after administration and a peak response 10 min after administration. Pretreatment with L-dopa (30 mg/kg) 30 min before administration of MCP suppressed the early PA response to MCP. PRA after MCP showed no change at 5 min but increased significantly at 10 min, with peak responses occurring at 30 min. Preadministration of L-dopa blunted and delayed the PRA response to MCP. Preadministration of the angiotensin-converting enzyme inhibitor, SQ 14,225 (1 mg/kg), did not inhibit the PA response to MCP. Infusion of the angiotensin II antagonist, saralasin (10 micrograms/kg min-1), begun 30 min before MCP, depressed basal levels of PA slightly but did not significantly alter the PA response to MCP. Rats studied 36 h after bilateral nephrectomy displayed intact PA responses to MCP, but there was no PRA response to MCP. The results indicate that dopaminergic modulation of PA secretion occurs independently of alterations in renin secretion.
D000450:Aldosterone / Q000378:metabolism*; D000818:Animals; D018492:Dopamine Antagonists; D007700:Kinetics; D007980:Levodopa / Q000494:pharmacology*; D008297:Male; D008787:Metoclopramide / Q000494:pharmacology; D009392:Nephrectomy; D051381:Rats; D012083:Renin / Q000378:metabolism*
D018492:Dopamine Antagonists; D007980:Levodopa; D000450:Aldosterone; D012083:Renin; D008787:Metoclopramide