The effect of luteinizing hormone releasing hormone (LHRH) on progesterone and estradiol production was studied in human luteal tissue. Tissue slices were incubated in Ham's F-10 medium under an atmosphere of 95% O2: 5% CO2 at 37 degrees C for 4 h. Slices were treated with or without human chorionic gonadotropin (HCG) in the presence or absence of LHRH. HCG stimulated progesterone and estradiol production by human luteal tissue in a time- and dose-related manner. LHRH stimulated the basal progesterone production in five (one early luteal and four mid-luteal) of 17 corpora lutea, and stimulated the basal estradiol production in three (all mid-luteal) of 16 corpora lutea. On the other hand, LHRH inhibited HCG-stimulated progesterone production in four (two early luteal and two mid-luteal) of 22 corpora lutea, and inhibited HCG-stimulated estradiol production in four (one early luteal and three mid-luteal) of 18 corpora lutea. In the acute short-term incubations of human luteal tissue, therefore, LHRH had little effect on basal and HCG-stimulated steroidogenesis. However, in a few corpora lutea taken in the early or mid-luteal phase, LHRH stimulated basal steroidogenesis and inhibited HCG-stimulated steroidogenesis.
In vitro production of progesterone and estradiol by human corpora lutea of different ages was evaluated in the presence or absence of human chorionic gonadotrophin (HCG). Progesterone production by the luteal tissue was enhanced by as little as 0.1 IU/ml HCG and maximally stimulated by approximately 10 IU/ml HCG. Estradiol production was enhanced by 100 IU/ml HCG. Under control conditions, the synthetic activities of progesterone and estradiol were highest in the luteal tissue isolated from the mid-luteal phase corpora lutea and were lowest in the late luteal phase corpora lutea. The addition of HCG (100 IU/ml) stimulated progesterone and estradiol production by early and mid-luteal phase corpora lutea, whereas HCG had no effects on steroidogenesis by late luteal phase corpora lutea. The results suggest that the age of the corpus luteum might be an important factor governing luteal cell responsiveness to gonadotrophins.
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