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  • Title: Role of progesterone in regulating the effect of estradiol on the secretion of thyrotropin-releasing hormone and dopamine into hypophysial portal blood in ovariectomized rats.
    Author: Huang SW, Tsai SC, Tung YF, Wang PS.
    Journal: Neuroendocrinology; 1995 May; 61(5):536-41. PubMed ID: 7617131.
    Abstract:
    In this study, an investigation was undertaken regarding the effects of estradiol and progesterone on the secretion of thyrotropin-releasing hormone (TRH) and dopamine into hypophysial portal blood and on the concentrations of arterial plasma thyroid-stimulating hormone (TSH) and prolactin (PRL) in ovariectomized (Ovx) rats. Ovx rats were injected subcutaneously with either estradiol benzoate (25 micrograms/kg BW/day) or progesterone (10 or 50 mg/kg BW/day), or both estradiol benzoate and progesterone daily for 3 days. The control group was injected with sesame oil. The hypophysial portal blood was collected and mixed either with or without 2,3-dimercaptopropanol before extraction by methanol for measuring TRH or by perchloric acid for measuring dopamine. The femoral arterial blood was also collected. The concentrations of TRH in hypophysial portal plasma and that of PRL and TSH in femoral arterial plasma were measured by radioimmunoassay. The concentrations of catecholamine in portal plasma were measured by radioenzymatic assay. Concomitant estradiol benzoate and progesterone caused a dose-dependent increase in TRH concentration in portal plasma and that of PRL in arterial plasma in Ovx rats. Progesterone alone did not alter the concentration of portal plasma TRH and the concentration of arterial plasma PRL, but rather increased the concentrations of dopamine in the hypophysial portal plasma. These above results indicated that the increase in plasma PRL and TSH levels is associated with a rise in hypophysial portal plasma dopamine and TRH following injection of both progesterone and estradiol benzoate. We can conclude that stimulation of progesterone on the secretion of hypothalamic TRH is involved in the increase in plasma PRL following concomitant treatment of estradiol.
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