title: [The role of desensitization of glucocorticoid receptors in the development of vascular resistance to endogenous vasoconstrictors in traumatic shock].
abstract: The fact that the activity of cytosol glucocorticoid receptors decreases in shock have been shown before [Golikov P. P. et al., 2001]. The connection between the development of vascular hyporeactivity to endogenous vasoconstrictors and desensitization of glucocorticoid receptors was studied in this investigation. On Kenton traumatic model in a rat experiment, it was shown that the strength of the isometric constriction of the isolated aorta in response to angiotensin II, endothelin-1, phenylephrine, noradrenaline, and vasopressin falls on the second day after a severe mechanical injury (3.3, 2.1, 1.7, 1.6, and 1.5 times, respectively; p < 0.01). On the contrary, the strength of the constriction in response to serotonin increases more then twice. Artificial desensitization of glucocorticoid receptors by long-term administration of dexamethasone (3 mg per kg during five days) results in similar changes of vascular reactivity i.e. a 2.5, 2, 7, and 1.4-fold decrease in the strength of aortal constriction in response to angiotensin II, vasopressin, and endothelin-1, respectively. The strength of the constriction in response to serotonin tended to increase as well. Carbahol-induced relaxation of the aorta pre-constricted with noradrenaline did not change compared with control, being 70 to 80%, both in shock and after desensitization of glucocorticoid receptors with dexamethasone. Presumably, the pathogenetic mechanism of pressor reaction suppression, connected with a decrease in cytosol glucocorticoid receptor activity and thus with inhibition of glucocorticoid-induced expression of the membrane receptors of endogenous vasoconstrictors, is realized in traumatic shock together with other mechanisms.
authors: L M
authors: LM
authors: Kozhevnikova
authors: P P
authors: PP
authors: Avdonin
authors: I F
authors: IF
authors: Sukhanova
authors: P V
authors: PV
authors: Avdonin
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D003907:Dexamethasone / Q000494:pharmacology*; D004195:Disease Models, Animal; D005938:Glucocorticoids / Q000494:pharmacology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D011965:Receptors, Glucocorticoid / Q000037:antagonists & inhibitors* / Q000378:metabolism; D012774:Shock, Traumatic / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects*
chemical_list: D005938:Glucocorticoids; D011965:Receptors, Glucocorticoid; D003907:Dexamethasone