title: Spironolactone: a glucocorticoid agonist or antagonist?
abstract: Spironolactone displaces 3H-dexamethasone from HTC cell nuclei and inhibits the induction of tyrosine aminotransferase (TAT) activity by dexamethasone in HTC cells. Spironolactone alone fails to increase TAT activity in HTC cells or in the liver of adrenalectomized rats. These actions indicate that spironolactone lacks glucocorticoid agonist activity but can be an antagonistic to the actions of glucocorticoid as well as mineralocorticoid steroid hormones.
mesh_terms: D000315:Adrenalectomy; D000818:Animals; D002460:Cell Line; D002467:Cell Nucleus / Q000378:metabolism; D003907:Dexamethasone / Q000378:metabolism* / Q000494:pharmacology; D004790:Enzyme Induction / Q000187:drug effects; D008114:Liver Neoplasms, Experimental / Q000378:metabolism; D008297:Male; D051381:Rats; D011965:Receptors, Glucocorticoid / Q000187:drug effects / Q000378:metabolism*; D011987:Receptors, Steroid / Q000378:metabolism*; D013148:Spironolactone / Q000494:pharmacology*; D014444:Tyrosine Transaminase / Q000096:biosynthesis*
chemical_list: D011965:Receptors, Glucocorticoid; D011987:Receptors, Steroid; D013148:Spironolactone; D003907:Dexamethasone; D014444:Tyrosine Transaminase