Stimulation of the primate corpus luteum (CL) by endogenous CG in early pregnancy or by exogenous human CG (hCG) in simulated early pregnancy, is transient, despite continued exposure to rising concentrations of CG. The objective of this study was to determine if the transitory response of the CL to CG is related to changes in gonadotropin receptors. Numbers and affinities of available LH/CG binding sites were characterized in the CL of rhesus monkeys (n = 27) during prolonged CG exposure in simulated early pregnancy, and the temporal relationship between changes in receptor parameters and in luteal function was examined. Administration of hCG increased progesterone concentrations above pretreatment levels within 9 h (2.2 ± 0.8 vs. 7.6 ± 1.1 ng/ml, mean ± us, P < 0.05); the relative increase (345% of control) in serum progesterone was more profound than that of available hCG binding sites (135%, P > 0.05) or luteal weight (128%, P > 0.05) over this interval. Receptor affinities for hCG remained comparable to pretreatment values (Kd = 1.1 ± 0.2 × 10-10 M) throughout this 9-h period. A significant diminution in available hCG receptors occurred between 9 h (12.7 ± 2.1 fmol/mg tissue) and 3 days (7.4 ± 1.5 fmol/mg tissue) of hCG treatment (P < 0.05). The loss of available CG receptors preceded a significant decline in serum progesterone concentrations. Serum progesterone decreased by 6 days (4.0 ± 0.6 ng/ml, P < 0.05) of hCG treatment, as did receptor affinity for hCG (Kd = 4.7 ± 0.9 × 10-10 M, P < 0.05). Numbers and affinities of available receptors for hCG and serum progesterone concentrations fell before any decrease in luteal weight. Binding capacities and receptor affinities for human LH were comparable to those for hCG throughout simulated early pregnancy. In conclusion, the population of available LH/ CG receptors in the macaque CL is maintained, or perhaps modestly increased, amidst dramatic stimulation of luteal function during early CG exposure. The subsequent diminution of number and affinity of available LH/CG receptors during prolonged exposure to CG in early pregnancy may compromise CL function and thus participate in the establishment of the transient nature of the luteal response to CG.
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