title: Effect of stress-like concentrations of cortisol on the feedback potency of oestradiol in orchidectomized sheep.
abstract: The effect of stress-like concentrations of cortisol on oestradiol-induced change in LH secretion and GnRH receptor expression was evaluated in orchidectomized sheep (wethers). Twenty-four wethers were assigned at random to one of the four treatment groups in a 2x2 factorial design (n=6 wethers/group). Wethers received cortisol (90 microg/kg/h; groups 2 and 4) or a comparable volume of cortisol delivery vehicle (groups 1 and 3) by continuous infusion for 48 h. During the final 24 h of infusion, wethers received oestradiol (6 ng/kg/h; groups 3 and 4) or oestradiol delivery vehicle (groups 1 and 2). The pattern of LH secretion was assessed during a 3-h period of intensive blood collection beginning 21 h after initiation of oestradiol infusion. Although neither cortisol nor oestradiol alone affected (P>0.05) mean serum concentration of LH or LH pulse frequency, serum LH and the frequency of secretory episodes of LH were significantly reduced (P<0.05) in wethers receiving cortisol and oestradiol in combination. Anterior pituitary tissue was collected at the end of the infusion period. Oestradiol increased (P<0.05) tissue concentrations of GnRH receptor and GnRH receptor mRNA. Although cortisol alone did not affect (P>0.05) basal concentrations of receptor or receptor mRNA, the magnitude of oestradiol-induced increase in GnRH receptor and GnRH receptor mRNA was significantly reduced in wethers receiving cortisol and oestradiol concurrently. Conversely, steady-state concentrations of mRNA encoding the LHbeta and FSHbeta subunits were increased (P<0.05) in wethers receiving cortisol. These observations demonstrate that stress-like concentrations of cortisol act in concert with oestradiol to suppress LH secretion. In addition, cortisol blocks oestradiol-dependent increase in pituitary tissue concentrations of GnRH receptor and GnRH receptor mRNA.
authors.affiliation: Department of Animal Science, University of California, Davis, CA 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 / Q000097:blood / Q000494:pharmacology*; D005246:Feedback; D005640:Follicle Stimulating Hormone / Q000097:blood / Q000378:metabolism; D006854:Hydrocortisone / Q000097:blood* / Q000494:pharmacology; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism; D008297:Male; D009919:Orchiectomy; D010903:Pituitary Gland, Anterior / Q000187:drug effects / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011966:Receptors, LHRH / Q000235:genetics / Q000378:metabolism; D012756:Sheep / Q000097:blood*; D013312:Stress, Physiological
chemical_list: D012333:RNA, Messenger; D011966:Receptors, LHRH; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D006854:Hydrocortisone