Effect of temperature on α2‐ and α1‐adrenoceptor‐mediated responses in the pithed rat and in the rat vena cava

Publisher Website
Google Scholar
Abstract
The influence of body temperature on the .alpha.1- and .alpha.2-adrenoceptor-mediated pressor responses has been investigated in the pithed rat. The pressor responses to noradrenaline, to the full .alpha.1-adrenoceptor agonists phenylephrine and cirazoline and to tyramine were not influenced by lowering the temperature from 36-37.degree.C to 27-29.degree.C. In contrast, the dose-response curves for the pressor effects of the partial .alpha.1-adrenoceptor agonist ST 587 and of the .alpha.2-adrenoceptor agonist B-HT 920 (2-amino-6-allyl-5,6,7,8-tetrahydro-4H-thiazolo-[4,5-d]-azepine), B-HT 933 (2-amino-6-ethyl-5,6,7,8-tetrahydro-4H-[4,5-d]azepine), clonidine, moxonidine and M-7 (2-dimethylamino-5,6-dihydroxy-1,2,3,4-tetrahydronaphthalene hydrobromide) were markedly depressed (without change in the ED50 values), when the body temperature was lowered from 36-37.degree.C to 27-29.degree.C. After i.v. administration of yohimbine, there was a rightward shift of the dose-response curve for B-HT 920, and the degree of this shift was the same at all temperatures investigated. In the rat vena cava preincubated with [3H]-noradrenaline, the B-HT 920-induced .alpha.2-adrenoceptor-mediated inhibition of electrically evoked tritium overflow was also reduced at lower temperature. These results are compatible with the suggestion that cooling decreases the .alpha.2-adrenoceptor-mediated pre- and postsynaptic responses in the rat vena cava and pithed rat respectively, leaving the pressor effect induced by full, but not partial .alpha.1-adrenoceptor agonists in the pithed rat unaffected.