Pharmacological Analysis of Vasodilator Responses to Alpha2-Adrenoceptor Agonists in Isolated Rat Common Carotid Arteries

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Abstract
Using the cannula inserting method, vasodilator responses to alpha2-adrenoceptor agonist (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 .gtoreq. 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 PGF2.alpha., 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 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.