Pharmacological study of cholinergic mechanisms of compensatory ovarian hypertrophy in rats.
Treatment of hemicastrated adult female rats with nicotine increased the compensatory ovarian hypertrophy (COH) while central n-cholinolytic IEM-506 decreased COH and prevented the estrogen-induced suppression of COH. Administration of L-DOPA abolished the effect of IEM-506, and disulfiram blocked gonadotropic action of nicotine. Elevation of the dose of arecoline decreased COH and the sensitivity of hypothalamo-gonadotropic complex to estrogen suppression. Treatment of rats with L-DOPA and disulfiram abolished the late effect of arecoline. Central m-cholinolytic metamizyl decreased COH, potentiated the effect of estrogen and prevented the gonadotropic effect of L-DOPA. The regulatory role of m-cholinergic systems in noradrenaline mediation of gonadotropic function and n-cholinergic system in dopamine ones are suggested.
D000818:Animals; D001115:Arecoline / Q000494:pharmacology; D001535:Benactyzine / Q000031:analogs & derivatives / Q000494:pharmacology; D002369:Castration; D004054:Diethylstilbestrol / Q000494:pharmacology; D004158:Diphenylacetic Acids / Q000031:analogs & derivatives / Q000494:pharmacology; D004221:Disulfiram / Q000494:pharmacology; D005260:Female; D006984:Hypertrophy; D007980:Levodopa / Q000494:pharmacology; D009538:Nicotine / Q000494:pharmacology; D010053:Ovary / Q000473:pathology*; D010276:Parasympatholytics / Q000494:pharmacology*; D010277:Parasympathomimetics / Q000494:pharmacology*; D051381:Rats
D004158:Diphenylacetic Acids; D010276:Parasympatholytics; D010277:Parasympathomimetics; C002675:ethyldiphacil; D007980:Levodopa; D001115:Arecoline; D001535:Benactyzine; D009538:Nicotine; D004054:Diethylstilbestrol; D004221:Disulfiram