Attenuated In Vivo Progesterone Secretion by Ovine Corpora Lutea After Exposure to Luteinizing Hormone

Abstract

Exogenous gonadotropin releasing hormone (GnRH) and its agonistic analogs appear to display a marked antigonadotropic activity, interfering with luteinizing hormone (LH)-in-duced synthesis of progesterone by the developing corpus luteum in a variety of species (1). In cattle, administration of GnRH has been shown to reduce serum progesterone concentrations during the estrous cycle without causing luteal regression (2,3). This action of GnRH appears to be linked to the downregulation of luteal LH receptors (3). Loss of LH receptors and subsequent gonadal desensitization following treatment with GnRH was initially attributed to GnRH-induced release of LH (4). However, the presence of high-affinity binding sites for GnRH in the ovaries of the rat (5) and the antisteroidogenic effect of this decapeptide in hypophysectomized rats (6) has implicated a possible direct action of GnRH on the mammalian ovary. Recently, an ovarian protein (GLOH) which binds to rat GnRH receptors has been isolated from the ovaries of the ewe and the cow (7). While gonadal GnRH receptors have been identified in the rat, specific binding sites for this decapeptide have not been found in domestic species (8). Therefore, the mechanism by which GnRH reduces luteal steroidogenesis in domestic species remains enigmatic.