Estradiol-17 beta (E) rapidly (5-12h) induced ovine pituitary cultures to increase their binding for des-Gly10-(D-Ala6)-GnRH ethylamide by 2.5 to 4.5-fold. The ED50 for E was near 0.1 nM. Scatchard analysis indicated the E increased binding by increasing receptors for gonadotrophin releasing hormone (GnRH). GnRH-stimulated release of luteinizing hormone (LH) increased 2-fold along with the increase in GnRH receptors but heightened responsiveness to GnRH disappeared after 27h of E-treatment even though GnRH receptors remained elevated. These data are consistent with the concept that: (1) E increased GnRH receptors which initially enhanced gonadotroph responsiveness to GnRH, and (2) E subsequently nullified the increased response to GnRH by blocking a mechanism of LH secretion not associated with GnRH receptor number. Further support for this hypothesis came from studies with porcine follicular inhibin. Inhibin, in ovine pituitary culture, concomitantly increased GnRH receptors by 5-fold and GnRH-stimulated LH secretion by 2-fold. Inhibin maintained both effects long term (48h).