Dissociation of Two Distinct Luteotropic Effects of Prolactin: Regulation of Luteinizing Hormone-Receptor Content and Progesterone Secretion during Pregnancy*

Abstract

The roles of the pituitary and placenta in pregnant rats and the effects of prolactin and rat placental lactogen on luteal cell function were examined. Hypophysectomy, but not hysterectomy, on day 9 of pregnancy caused serum progesterone concentrations to decrease 90% and luteal cell LH [luteinizing hormone] receptor content to drop 35% by 24 h suggesting pituitary support of luteal cell function at this time. Hypophysectomy and hysterectomy on day 9 effected a similar change in progesterone. The decrease in LH receptor, which was not seen until 48 h, was prevented by daily administration of prolactin (250 .mu.g/day) or serum of day 12 pregnant rats (2 ml/day) [PRS]. The drop in progesterone production was reduced by the administration of prolactin or PRS alone but was completely prevented by combining prolactin treatment with estradiol (100 .mu.g/day in sesame oil). Hysterectomy on day 12 of pregnancy caused serum progesterone to decrease within 72 h. LH receptor content remained unchanged on day 15 of pregnancy, but dropped significantly by day 18. After hypophysectomy on day 12 of pregnancy, serum progesterone remained elevated through day 22 and luteal cell LH receptor content increased significantly. After hysterectomy and hypophysectomy on day 12 of pregnancy, LH receptor remained elevated through day 16. During this period estradiol alone maintained progesterone production suggesting a sustaining effect of the midgestation peak of rat placental lactogen for 4 days. To maintain LH receptor content beyond day 16, daily injections of PRS were required. LH receptor content in corpora lutea and luteal cell progesterone production are regulated by the pituitary in the 1st half of pregnancy and by the placenta thereafter. In the pregnant rat prolactin or prolactin-like hormones plus estradiol appear to form the luteotropic complex.