Effect of Progesterone on Pituitary and Ovarian Responsiveness to Placental Gonadotrophins1

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Abstract
The presence of the pituitary gland enhanced ovarian responsiveness (as measured by induction of ovulation) to exogenously administered placental gonado-tropins in the immature rat. This effect can be explained on the basis of PMS [pregnant mares serum] causing the release of FSH [follicle-stimulating hormone] and LH [luteinizing hormone] from the pituitary gland. HCG [human chorionic gonadotropin] (5 IU injected sub-cutaneously 56 hr. following a similar injection of 30 IU PMS) exerted no additional effect on endogenous gonadotropin release. However, greater ovarian responsiveness to HCG was observed in intact than in hypophysectomized rats as a result of the action of PMS via the pituitary gland. Progesterone (4 mg/day x 3), when superimposed on PMS (30 IU) or PMS (30 IU) followed 56 hr. later by HCG (5 IU), had no significant effect on plasma or pituitary LH levels. However, progesterone blocked the release of FSH caused by PMS, whether PMS was given alone or followed by HCG treatment. This effect was accompanied by a decrease in ovarian nucleic acid content and the number of ova released. Thus, progesterone can block only 1 of the 2 actions of PMS on the pituitary. In the above treatment regimen, HCG acted only at the level of the ovary. Its action was not directly inhibited by progesterone since this steroid did not affect ovulation induced with PMS-HCG (or PMS-LH; FSH-LH) treatment in the hypophysectomized animal. These observations indicate that progesterone cannot influence ovarian responsiveness to placental (or pituitary) gonadotropins at the target organ, but rather acts by blocking the release of endogenous FSH.