Evidence that a factor besides progesterone, prolactin, or plasma-estradiol-binding protein inhibits estrogen-induced sexual receptivity in pregnant rats.

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Abstract
Daily administration of estradiol benzoate stimulated significantly less lordotic behavior in rats during the 2nd half of pregnancy than in ovariectomized females that received s.c. progesterone implants, pituitary grafts that raised plasma prolactin, or both treatments combined. Following an initial facilitation of receptivity, females with progesterone implants showed only moderate reductions in lordosis quotients over 3 test days. The capacity of plasma from pregnant rats to bind estradiol increased significantly during the 2nd half of pregnancy. Daily administration to pregnant rats of a synthetic estrogen, R 2858 [methoxyethynylestradiol], which is not bound by plasma protein, was more effective than estradiol benzoate in stimulating receptive behavior. Administration of estradiol benzoate also stimulated significantly lower levels of sexual behavior in pregnant females than in females in which pseudopregnancy had been prolonged by previous hysterectomy or induction of uterine decidualization. Some endocrine factor other than progesterone, prolactin or estradiol-binding protein may be primarily responsible for the potent suppression of behavioral responsiveness to estrogen which occurs in pregnant rats. Possibly 5.alpha.-reduced androgens may cause these behavioral effects.