A possible role for endogenous glucocorticoids in orchiectomy-induced atrophy of the rat levator ani muscle: studies with RU 38486, a potent and selective antiglucocorticoid.
We employed RU 38486, a potent and selective antiglucocorticoid, to study a possible role for endogenous glucocorticoids in atrophy of the levator ani muscle secondary to castration of male rats. RU 38486 was shown to block [3H]triamcinolone acetonide binding to cytosol from levator ani muscle. Daily oral administration of RU 38486 to castrated rats partially prevented atrophy of the levator ani muscle, as well as a decrease in RNA concentration. In a control group receiving RU 38486 alone, the levator ani underwent significant (20%) hypertrophy. Administration of exogenous dexamethasone also caused pronounced atrophy of the levator ani muscle. This atrophy was prevented, to a significant degree, by simultaneous oral administration of RU 38486. It is concluded that endogenous glucocorticoids, the actions of which are blocked by RU 38486, may be involved in regulation of the mass of the levator ani muscle in intact rats.
D000818:Animals; D001284:Atrophy / Q000139:chemically induced; D001835:Body Weight / Q000187:drug effects; D003907:Dexamethasone / Q000494:pharmacology; D004963:Estrenes / Q000494:pharmacology*; D005938:Glucocorticoids / Q000502:physiology*; D008297:Male; D015735:Mifepristone; D009132:Muscles / Q000473:pathology / Q000502:physiology*; D009919:Orchiectomy; D051381:Rats; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D013997:Time Factors; D014222:Triamcinolone Acetonide / Q000378:metabolism
D004963:Estrenes; D005938:Glucocorticoids; D011965:Receptors, Glucocorticoid; D015735:Mifepristone; D003907:Dexamethasone; D014222:Triamcinolone Acetonide