Rat placental hormones: attempts for identification of rat chorionic gonadotrophin and rat placental lactogen by in vivo experiments

Abstract. Rat placental extracts (rPE) were investigated in bioassays for their possible content of rat placental lactogen (rPL) and rat chorionic gonadotrophin (rCG). Luteotrophic and lactogenic activity of rPL was assessed by substitution of rats depleted of endogenous prolactin (Prl) by means of bromoergocryptine (BEC) in early pregnancy and the period of lactation, respectively. The abortifacient effect of a single dose of BEC on day 6 of pregnancy was abolished by rPE equivalent to 1 g rat placenta corresponding to 5 IU bovine Prl (NIH-P-B 2). Substitution was necessary until the evening of day 7 indicating that rPL does not take over the function of Prl before day 8. During lactation rPE reversed the lactation inhibiting effect of daily BEC treatment. In this assay rPL activity corresponded to 1.25–2.5 IU bPrl/g placenta. In order to test for the possible existence of rCG the gonadotrophic activity of rPE was assessed in immature female mice. No gonadotrophic activity was found when rPE equivalent to 1 g rat placenta was administered, whereas equivalents of 3 mg human placenta and 12 mg rat pituitary entailed a dose-dependent response. In this system 0.12 IU human chorionic gonadotrophin (hCG), which served as standard, was the minimal dose (MD) resulting in increased uterine weight. In addition rPE was tested in the immature female rat, where the limit of detection was found to be 0.5 IU hCG. Again no gonadotrophic activity was found in rPE. As the effects of rCG might have been restricted to its presumed target, the corpus luteum of pregnancy, rPE was also tested in pregnant rats depleted of endogenous luteinizing hormone (LH) by a single injection of anti-LH antibodies on day 10 of pregnancy. A MDof 0.5 IU hCG, which served as standard, prevented resorption of foetuses in all animals tested. rPE equivalent to 3.5 g rat placenta, rat pregnancy serum of day 18 and placental transplants could not substitute for endogenous LH.