Cyproheptadine and mineralocorticoid effector mechanisms.
Cyproheptadine has recently been reported to blunt the furosemide-induced rise in PRA in normal subjects and to acutely lower plasma aldosterone levels in patients with hyperaldosteronism due to bilateral adrenal hyperplasia; both actions have tentatively been ascribed to the antiserotoninergic action of the drug. We here describe receptor studies showing cyproheptadine to occupy mineralocorticoid, but not glucocorticoid, receptors in rat and mouse kidney. On bioassay, cyproheptadine is a partial mineralocorticoid agonist/predominant antagonist.
D000315:Adrenalectomy; D000450:Aldosterone / Q000378:metabolism; D000818:Animals; D001681:Biological Assay; D003533:Cyproheptadine / Q000378:metabolism* / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004594:Electrophysiology; D005260:Female; D007668:Kidney / Q000378:metabolism*; D008297:Male; D051379:Mice; D000451:Mineralocorticoid Receptor Antagonists; D051381:Rats; D011919:Rats, Inbred Strains; D018161:Receptors, Mineralocorticoid; D011987:Receptors, Steroid / Q000378:metabolism*; D012007:Rectum / Q000187:drug effects / Q000502:physiology
D000451:Mineralocorticoid Receptor Antagonists; D018161:Receptors, Mineralocorticoid; D011987:Receptors, Steroid; D003533:Cyproheptadine; D000450:Aldosterone