The effects of gonadotropin on the phosphatidylinositol pathway in the primate corpus luteum.

The current study was designed to investigate the effects of gonadotropin on basal and prostaglandin (PG) F2 alpha-induced activity of the phosphatidylinositol pathway in corpora lutea (CL) of rhesus monkeys. Luteal progesterone production in vitro was significantly stimulated (P < 0.05) by human chorionic gonadotropin (hCG). Neither basal nor PGF2 alpha-induced phosphatidylinositol 4,5-bisphosphate hydrolysis was significantly influenced by hCG in CL of various ages (P > 0.10). Gonadotropin did induce a slight, yet sustained, increase (P < 0.05) in [Ca2+]i in approximately 70% of luteal cells. The maximal increase in [Ca2+]i in response to hCG (approximately 100 nM) was about one-tenth that induced by PGF2 alpha (approximately 1000 nM). hCG treatment did not alter (P > 0.10) the increase in [Ca2+]i induced by PGF2 alpha Treatment-induced changes in [Ca2+]i did not differ between small (17-21 microns) and large (23-28 microns) luteal cells. Therefore, luteolytic agents are more potent activators of the phosphatidylinositol pathway than luteotropins. This is consistent with the hypothesis that the phosphatidylinositol pathway is involved in primate luteal regression. The inability of hCG to acutely alter the responsiveness of this pathway to PGF2 alpha suggests that CG may rescue the CL of early pregnancy via a mechanism other than direct inhibition of the luteolytic actions of PGF2 alpha.