PHARMACOLOGICAL ANALYSIS OF VASODILATOR RESPONSES TO ALPHA-2-ADRENOCEPTOR AGONISTS IN ISOLATED RAT COMMON CAROTID ARTERIES

Using the cannula inserting method, vasodilator responses to alpha2-adrenoceptor agonists (clonidine, guanabenz, DJ7141 and xylazine) were investigated in isolated and perfused rat common carotid arteries. Alpha2-adrenoceptor agonists dose-dependently induced a vasodilation in preparations preconstricted by noradrenaline. The potencies were in the order of clonidine>guanabenz>DJ-7141≥xylazine. Removal of the endothelium inhibited ACh-induced vasodilation, but not the alpha2-agonist-induced dilation. Atropine treatment inhibited ACh-induced vasodilation, but not the alpha2-agonist-induced dilation. Alpha2-agonist-induced dilations were not modified by beta-blockade, which significantly ? suppressed isoprenaline-induced vasodilations. The potent alpha2-adrenoceptor antagonist DG5128 did not influence the alpha2-agonist-induced vasodilation. In preparations preconstricted by PGF2α, clonidine and xylazine never induced a vasodilation, and clonidine frequently induced vasoconstrictions that were completely blocked by bunazosin. It is concluded that alpha2-adrenoceptor agonist-induced vasodilation is independent from the existence of the endothelium, and that it is not related to vascular beta-and alpha2-adrenoceptors and muscarinic receptors, suggesting that the alpha2-adrenoceptor agonist-induced vasodilation is due to an antagonistic activity towards the vascular alpha1-adrenoceptors. © 1990, The Japanese Pharmacological Society. All rights reserved.