title: [Medicinal activation and inhibition of function of glucocorticoid receptors as the basis for regulation of the glucocorticoid effect].
abstract: On the basis of Scatchard and Lineweaver-Burk analysis, it was demonstrated that a series of drugs either activated or inhibited the function of types II and III glucocorticoid receptors. Analgine (0.04-10.0 mM) and sodium salicylate (12.5-50.0 mM) suppress the type II glucocorticoid receptor function of rat liver cytosol. Maradol (5.0 mM) increases the type II glucocorticoid receptors density but decreases the measurable constant for the [3H]acetonide triamsinolone interaction with type II glucocorticoid receptors. Analgine (1.25-10.0 mM) and sodium salicylate (0.62-10.0 mM) increase the type III glucocorticoid receptor function of rat liver cytosol. Maradol (0.25-1.0 mM) suppresses the type III glucocorticoid receptor function. The mechanism of regulation of the glucocorticoid effect by nonsteroid drugs influencing upon the function of types II and III glucocorticoid receptors is discussed.
authors.forename: P P
authors.initials: PP
authors.lastname: Golikov
mesh_terms: D000818:Animals; D016718:Arachidonic Acid / Q000494:pharmacology; D001665:Binding Sites; D002077:Butorphanol / Q000494:pharmacology; D003600:Cytosol / Q000187:drug effects / Q000378:metabolism; D004177:Dipyrone / Q000494:pharmacology; D005938:Glucocorticoids / Q000502:physiology*; D007700:Kinetics; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D011965:Receptors, Glucocorticoid / Q000037:antagonists & inhibitors / Q000187:drug effects* / Q000378:metabolism; D012980:Sodium Salicylate / Q000494:pharmacology; D014221:Triamcinolone / Q000378:metabolism / Q000494:pharmacology
chemical_list: D005938:Glucocorticoids; D011965:Receptors, Glucocorticoid; D014221:Triamcinolone; D016718:Arachidonic Acid; D004177:Dipyrone; D002077:Butorphanol; D012980:Sodium Salicylate
vernacular_title: Lekarstvennoe aktivirovanie i ingibirovanie funktsii gliukokorticoidnykh retseptorov kak osnova reguliatsii gliukokortikoidnogo éffekta.