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.