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Direct Inhibition by Ergocornine of Pituitary Prolactin Release
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1971
Year
Human GrowthPituitary TransplantGynecologyPharmacotherapyFemale Reproductive FunctionAnterior PituitaryReproductive EndocrinologyPituitary GlandNeuroendocrine MechanismReproductive MedicinePituitary DiseasePublic HealthEndocrine MechanismNeuropharmacologyNervous SystemEndocrinologyPharmacologyPituitary Prolactin ReleasePhysiologyUterine ReceptivityMedicineEndocrine ResearchEstradiol Benzoate
The effects of ergocornine, estradiol benzoate (EB) or both on anterior pituitary (AP) and serum prolactin concentrations were studied in ovariectomized or hypophysectomized rats with a pituitary transplant, and directly on the AP in vitro. Injections of 5 or 10 μg EB into ovariectomized rats for 5 days produced 3-to 4-fold increase in AP prolactin concentration, a 6-to 8-fold rise in serum prolactin and increases in pituitary weight and mammary growth. Doses of 0.1 or 0.3 mg ergocornine methanesulfonate (ERG) partially or completely inhibited the stimulatory effects of EB on each of these parameters. Transplantation of one AP into the kidney capsule of hypophysectomizedovariectomized rats resulted in relatively high blood prolactin levels. ERG reduced prolactin release from the AP graft and mammary growth, whereas EB increased both AP and serum prolactin concentrations and mammary growth. When given together, ERG partially counteracted EB stimulation of pituitary and serum prolactin levels and mammary growth. In vitro studies showed that EB directly stimulated, whereas ERG inhibited, release and increased pituitary accumulation of prolactin. When both EB and ERG were added to the incubation medium, prolactin release was inhibited and AP prolactin concentration was increased. These results indicate that ergocornine can inhibit prolactin release by a direct action on the AP, and can counteract the stimulatory effect of estrogen on prolactin secretion. (Endocrinology89: 229, 1971)