Rivier C, Vale W
Clayton Foundation Laboratories for Peptide Biology, Salk Institute, La Jolla, California 92037.
Endocrinology. 1989 Jan;124(1):195-8. doi: 10.1210/endo-124-1-195.
To investigate the possibility that sex steroids and GnRH might act directly at the level of the ovary to modulate the secretion of immunoreactive inhibin, we have administered estradiol benzoate, PMSG, or GnRH analogs to immature (24-day-old) hypophysectomized female rats. The sc injection of 10-100 micrograms estradiol benzoate markedly (P less than or equal to 0.01) increased plasma inhibin levels measured 48 h later. Administration of the GnRH agonist [DTrp6,Pro9-NEt]GnRH significantly (P less than or equal to 0.05) inhibited both spontaneous and PMSG-induced inhibin secretion, while the GnRH antagonist [Ac-D2Nal1,D4ClPhe2,D3Pal3,Arg5,DGlu6(AA), DAla10]GnRH augmented the stimulatory effect of PMSG action on inhibin release. These results suggest a direct ovarian site of action of sex steroids and GnRH analogs in modulating the release of immunoreactive inhibin. They also support the hypothesis that an endogenous GnRH-like peptide of ovarian origin plays a physiological paracrine role in modulating inhibin secretion in the rat.