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Primary cultures of pituitary cells from adult female rats were exposed to increasing concentrations (10(-13) to 10(-6)M) of selected prostaglandins (PGE2, PGF2 alpha, PGI2, 6-keto-PGF1 alpha, and sulproston). The release of luteinizing hormone (LH) by the pituicytes was monitored. In a second series of experiments, pituitary cells were treated with prostaglandins as described above and additionally challenged with a submaximal stimulus of gonadotrophin-releasing hormone (GnRH; 10(-9) M). The spontaneous LH-release in all prostaglandin treated cultures did not differ from the controls. When stimulated with 10(-9) M GnRH, the LH-release increased approx. six-fold in all cultures, with no difference between prostaglandin treated cells and the respective controls. Thus, the prostaglandins tested - at least at concentrations less than or equal to 10(-6) M - have neither a direct positive or negative effect on pituitary LH-release, nor do they enhance or decrease the LH-releasing effect of GnRH. These prostaglandins are probably not involved in the cellular regulation of LH-release by the pituicyte.

Primary pituitary cell cultures from adult female rats were incubated for 4 or 24 h with various concentrations of estradiol (E2) or the antiestrogens (AE) tamoxifen (TMX), 4-hydroxytamoxifen (OH-TMX), and clomiphene citrate (CC). The luteinizing hormone (LH)-response of these cultures to gonadotrophin releasing hormone (GnRH) was monitored. Treatment for 4 or 24 h with high concentrations (10(-5) M) of the AE significantly decreased the GnRH-induced LH-release by the gonadotrophs. The negative E2-effect, which is observed in this model after 4 h was enhanced and the positive E2-effect, which occurs after 24 h, was completely reversed into a negative effect by these high AE-concentrations. Treatment of pituitary cells with increasing concentrations of E2 (10(-13)-10(-6) M) or AE (10(-12)-10(-5) M) for 24 h led first to a dose dependent increase of the LH-response to 5 X 10(-10) M GnRH. At higher E2- or AE-concentrations this positive effect was lost, resulting in bell shaped dose-response curves. The following maximal effective concentrations (EDmax) were found: E2 = 10(-10) M, OH-TMX = 10(-9) M, CC = 10(-7) M, TMX = 10(-6) M. Incubation of pituitary cells for 24 h with concentrations of AE near their EDmax and stimulation with increasing concentrations (10(-11)-10(-7) M) of GnRH resulted in significant increases of LH-secretion over a wide range of GnRH-concentrations. It is concluded that AE possess marked intrinsic activities on pituitary LH-secretion: at extremely high concentrations they suppress the GnRH-induced release of the gonadotrophin. At lower concentrations they increase the pituitary LH-response to GnRH in a manner which is qualitatively indistinguishable from that of E2.