title: Effect of stress-like concentrations of cortisol on gonadotroph function in orchidectomized sheep.
abstract: The effect of stress-like concentrations of cortisol (C) on the feedback potency of estradiol (E2) was assessed using 32 orchidectomized sheep (wethers) assigned at random to 1 of 4 treatment groups in a 2 x 2 factorial design. Wethers received C (3. 6 mg/50 kg per hour; groups 2 and 4) or a comparable volume of C delivery vehicle (groups 1 and 3) as a continuous infusion for 7 days. During the final 48 h of infusion, wethers received E2 (0.3 microg/50 kg/h; groups 3 and 4) or E2 delivery vehicle (groups 1 and 2). The pattern of LH secretion was assessed during a 4-h period of intensive blood collection beginning 44 h after initiation of E2 infusion. Gonadotroph responsiveness (LH secretion induced by GnRH challenge [500 ng, i.v.]) was determined 48 h after E2 delivery was begun. Although the frequency of secretory episodes of LH was not affected (p > 0.05) by infusion of C or E2 alone, LH pulse frequency was significantly decreased in wethers receiving C and E2 in combination. In contrast, neither the magnitude of basal gonadotroph responsiveness nor the extent of E2-dependent augmentation of responsiveness was significantly affected by stress-like concentrations of C. In a second experiment, the effect of C on the magnitude of E2-induced increase in pituitary concentration of GnRH receptor and GnRH receptor mRNA was assessed using 32 additional wethers. Continuous infusion of E2 for 48 h increased (p < 0.05) tissue concentrations of GnRH receptor and GnRH receptor mRNA. Concurrent delivery of C did not affect (p > 0.05) E2-induced increase in GnRH receptor mRNA but significantly reduced the magnitude of the E2-dependent increase in pituitary concentration of GnRH receptor. Collectively, these data indicate that stress-like concentrations of C enhance the negative feedback potency of E2 and reduce estrogen-dependent augmentation of the concentration of GnRH receptor in pituitary tissue.
authors.affiliation: Department of Animal Science, University of California, Davis, California 95616, USA.
authors.forename: C A
authors.initials: CA
authors.lastname: Daley
authors.forename: H
authors.initials: H
authors.lastname: Sakurai
authors.forename: B M
authors.initials: BM
authors.lastname: Adams
authors.forename: T E
authors.initials: TE
authors.lastname: Adams
mesh_terms: D000818:Animals; D004958:Estradiol / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology; D005246:Feedback; D005640:Follicle Stimulating Hormone / Q000097:blood; D015870:Gene Expression / Q000187:drug effects; D006065:Gonadotropins, Pituitary / Q000502:physiology*; D006854:Hydrocortisone / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*; D007700:Kinetics; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism; D008297:Male; D009919:Orchiectomy; D010902:Pituitary Gland / Q000187:drug effects / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011966:Receptors, LHRH / Q000235:genetics / Q000378:metabolism; D012756:Sheep / Q000502:physiology*; D013312:Stress, Physiological / Q000378:metabolism*
chemical_list: D006065:Gonadotropins, Pituitary; D012333:RNA, Messenger; D011966:Receptors, LHRH; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D006854:Hydrocortisone