title: Inhibition of corticosteroid-binding globulin caused by a severe stressor is apparently mediated by the adrenal but not by glucocorticoid receptors.
abstract: The effect of stress on serum corticosteroid-binding globulin (CBG) was studied in adult male Sprague-Dawley rats. CBG was measured either by a homologous radioimmunoassay (RIA) or by a binding assay (BA) using 3H-corticosterone. Exposure of adult male rats to a severe stressor such as immobilization (IMO) for 1 h did not alter serum CBG levels, but a significant decrease was found after 6 and especially 24 h IMO. This decrease was not observed after 24 h exposure to a milder treatment such as food and water deprivation. The effect of different periods of exposure to two stressors, IMO or restraint, was also studied. The following results were obtained:serum CBG levels were reduced by IMO, but only by restraint; IMO-induced reduction of CBG levels was always observed 24 h after starting exposure to IMO, independently of the actual period of exposure to the stressor; and IMO-induced inhibition of CBG was proportional to the hours of exposure to the stressor. Although IMO-induced inhibition of CBG was prevented by adrenalectomy, a role for glucocorticoid acting through their classical type II receptors is unclear as far as treatment of rats with the glucocorticoid receptor antagonist RU486 (100 mg/kg) did not prevent the inhibition caused by IMO. The present data clearly indicate that acute exposure to a stressor is able to decrease CBG levels provided that duration of exposure to the stressor and its intensity are high and that the effect is tested at least 6 h after the onset of stress. The effect appears to be mediated by some adrenal factor(s) other than glucocorticoids.
authors.affiliation: Departament de Biología Celular y de Fisiología, Facultad de Ciencias, Universidad Autónoma de Barcelona, Bellaterra, Spain.
authors.forename: O
authors.initials: O
authors.lastname: Martí
authors.forename: M
authors.initials: M
authors.lastname: Martín
authors.forename: A
authors.initials: A
authors.lastname: Gavaldà
authors.forename: M
authors.initials: M
authors.lastname: Giralt
authors.forename: J
authors.initials: J
authors.lastname: Hidalgo
authors.forename: B R
authors.initials: BR
authors.lastname: Hsu
authors.forename: R W
authors.initials: RW
authors.lastname: Kuhn
authors.forename: A
authors.initials: A
authors.lastname: Armario
mesh_terms: D000311:Adrenal Glands / Q000187:drug effects / Q000503:physiopathology*; D000315:Adrenalectomy; D000818:Animals; D003345:Corticosterone / Q000097:blood; D006727:Hormone Antagonists / Q000494:pharmacology; D007103:Immobilization; D008297:Male; D015735:Mifepristone / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011965:Receptors, Glucocorticoid / Q000187:drug effects / Q000502:physiology*; D013312:Stress, Physiological / Q000503:physiopathology*; D014156:Transcortin / Q000502:physiology*
chemical_list: D006727:Hormone Antagonists; D011965:Receptors, Glucocorticoid; D015735:Mifepristone; D014156:Transcortin; D003345:Corticosterone