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Short-term (0.5-4 h) treatment of rat pituitary cells in culture with estradiol (E2) results in a significant decrease of Gonadotropin-Releasing Hormone (GnRH) induced LH-release. We studied whether changes in the concentrations of GnRH-receptors (GnRH-R) might account for this phenomenon: pituitary cells from adult female rats were incubated for 4 or 24 h in the presence or absence of 10(-9) M E2. Then saturation curves of D-Ala6-des-Gly10-GnRH ethylamide binding were obtained. In addition, binding studies were carried out in cultures incubated for 0.5, 1, 2 or 4 h with or without 10(-9) M E2 using a near saturating concentration of GnRH-analog. No changes of GnRH-R affinity occurred (4 h experiments: Ka in vehicle treated cells: 0.94 +/- 0.2 x 10(9) M-1, Ka in E2 treated cells: 1.06 +/- 0.3 x 10(9) M-1; 24 h experiments: Ka vehicle: 0.95 +/- 0.2 x 10(9) M-1, Ka E2: 0.82 +/- 0.3 x 10(9) M-1). The GnRH-R concentrations, however, were significantly reduced (44 +/- 3%; P less than 0.001) by 4 h E2 treatment and increased (by 68 +/- 8%; P less than 0.01) by 24 h of E2 treatment. The GnRH induced LH-release in aliquots of the same cell preparations was significantly reduced after 4 h and markedly increased after 24 h of E2 treatment. The experiments on the time-course of the reduction of D-Ala6-GnRH-binding by E2 treatment showed that the number of GnRH-R was significantly decreased (24 +/- 1%; P less than 0.05) already after 0.5 h of exposure to the estrogen. This is also the time period after which the negative E2-effect on GnRH-induced LH-release becomes significant. These data provide first evidence that the short-term negative E2-effect on GnRH induced LH-release by rat pituitary cells in culture could be mediated via a reduction of available GnRH-R.

Several groups of endocrine manipulated prepuberal and young adult female rats were studied with the purpose of estimating the pituitary contribution to the uterine growth after a single injection of a physiological dose (1 μg/kg of body weight) of estradiol-17β (E 2 ). The different groups of E 2 and vehicle-injected animals included (a) castrated and (b) hypophysectomized and castrated (hypox) animals. In addition to these groups, a third represented by (c) hypox young adult female C 8 11RAP pituitary tumor-bearing rats were also studied to check whether this tumor behaves as the in situ pituitary present in castrated-only female rats. Results indicate that the pituitary of castrated rats and the rat pituitary tumor growing in the hypox rats significantly influence the increase of the wet and dry weights of the uterus following E 2 stimulation. It is proposed that there are uterotrophic factors in the pituitary and in the rat pituitary tumor tested.

Testosterone metabolism was studied in three cell clones (C 1 3RAP). C 2 9RAP and C 8 11RAP) established from an estradiol induced rat pituitary tumor. These cells were incubated with 5 or 50 ng/ml of tritiated testosterone for 2,6, 24 or 48 h in serum-free medium. The incubation medium were analysed for their content in tritiated dihydrotestosterone (DHT), 5α-androstanediols (diols) and 4-ene-androstenedione (Δ 4 ). In two clones (C 2 9RAP and C 8 11RAP) the cells metabolized very actively testosterone into DHT and diols since after 48 h of incubation 86% of testosterone were converted into 5α-reduced metabolites. This metabolism increased with testosterone concentrations and time of incubation. The third pituitary clone metabolized testosterone weakly in the same way than a normal kidney cell line used as a control.