title: Effects of repeated ether stress on the hypothalamic-pituitary-testes axis in adult rats with special reference to inhibin secretion.
abstract: Effects of ether stress on the hypothalamo-hypophysial-gonadal axis in adult male rats were examined. To clarify the role of adrenal glucocorticoids in gonadal function, the effects of adrenalectomy and Dexamethasone treatment were also investigated. Ether stress increased the plasma concentrations of ACTH and corticosterone, but decreased the plasma concentrations of LH, FSH, inhibin and testosterone. The pituitary responsiveness to LH-RH for LH release and testicular responsiveness to the endogenous LH for testosterone release were maintained in stressed rats. Adrenalectomy caused an increase in the plasma concentrations of ACTH, but decreased the plasma concentrations of LH, FSH and testosterone. Dexamethasone treatment in adrenalectomized rats recovered the levels of plasma gonadotropins to control levels. The concentration of plasma inhibin did not change in adrenalectomized rats, but it was decreased compared to control rats by Dexamethasone treatment. Treatments of Dexamethasone in intact male rats resulted in a decline in plasma levels of testosterone and inhibin without a decrease in the levels of LH and FSH, indicating the direct effect of Dexamethasone on the testes. These results indicate that increased ACTH secretion in stressed rats is probably due to hypersecretion of CRH from the hypothalamus, which suppresses gonadotropin secretion via the inhibition of LH-RH. The decreased levels of testosterone may be caused by a stress-induced decrease in plasma LH concentrations and increased secretion of corticosterone in the ether stressed rats. The low levels of plasma inhibin in stressed rats was also probably due to the direct effect of corticosterone on the Sertoli cells.
authors.affiliation: Laboratory of Veterinary Physiology, Tokyo University of Agriculture and Technology, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Tohei
authors.forename: T
authors.initials: T
authors.lastname: Tomabechi
authors.forename: M
authors.initials: M
authors.lastname: Mamada
authors.forename: M
authors.initials: M
authors.lastname: Akai
authors.forename: G
authors.initials: G
authors.lastname: Watanabe
authors.forename: K
authors.initials: K
authors.lastname: Taya
mesh_terms: D000315:Adrenalectomy; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000768:Anesthesia, General; D000818:Animals; D003345:Corticosterone / Q000097:blood; D003907:Dexamethasone / Q000494:pharmacology; D004986:Ether / Q000494:pharmacology*; D005640:Follicle Stimulating Hormone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000502:physiology*; D007265:Inhibins / Q000097:blood / Q000378:metabolism*; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological; D013737:Testis / Q000187:drug effects / Q000502:physiology*; D013739:Testosterone / Q000097:blood; D013997:Time Factors
chemical_list: D004986:Ether; D013739:Testosterone; D007265:Inhibins; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D003345:Corticosterone