[Glucocorticoid receptors and metabolic disorders of the liver and heart following immobilization].
A model of the immobilization stress aided to study the main characteristics of dexametasone-binding and transcortin-like receptors in the liver and heart cytosol, the level of endogenous corticosterone, induction of the glucocorticoid--dependent liver enzyme tyrosine aminotransferase (TATF), and amount of a number of metabolites. The study revealed disturbances of the receptor binding and cellular metabolism during the stress. A sharp increase of endogenous glucocorticoids in blood and tissues along with inhibition of the glucocorticoid receptor binding in organs and of the TATF activity, exhaustion of cellular contents of glucose and cholesterine, a decrease in the protein amount, increasing level of urine in blood and tissues as well as a considerable hyposodiumemia indicate transition of the stress from the compensated phase into the decompensated one.
D000818:Animals; D003345:Corticosterone / Q000378:metabolism; D003907:Dexamethasone / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D011965:Receptors, Glucocorticoid / Q000378:metabolism*; D011987:Receptors, Steroid / Q000378:metabolism*; D012149:Restraint, Physical / Q000009:adverse effects; D013312:Stress, Physiological / Q000378:metabolism*; D014444:Tyrosine Transaminase / Q000378:metabolism*
D011965:Receptors, Glucocorticoid; D011987:Receptors, Steroid; D003907:Dexamethasone; D014444:Tyrosine Transaminase; D003345:Corticosterone
Gliukokortikoidnye retseptory i metabolicheskie narusheniia v pecheni i serdtse pri immobilizatsii.