Vascular responses to beta-adrenoceptor subtype-selective agonists with and without endothelium in rat common carotid arteries.

1. Using the cannula inserting method, vasodilator responses to beta-adrenoceptor agonists (isoprenaline, denopamine and procaterol) were investigated in isolated and perfused rat common carotid arteries. 2. Each beta-adrenoceptor agonist induced a vasodilation in preparations preconstricted by phenylephrine in a dose-related manner. The potencies were in the order of isoprenaline > procaterol > denopamine. 3. Denopamine-induced dilations were significantly inhibited by 1 nmol betaxolol (a selective beta1-adrenoceptor antagonist), but it was not influenced by 1 nmol ICI 118,551 (a selective beta2-adrenoceptor antagonist). On the other hand, procaterol-induced vasodilations were significantly inhibited by 1 nmol ICI 118,551 but not modified by 10 nmol betaxolol. 4. ACh-induced vasodilations disappeared after intraluminal saponin injection to remove endothelium, but procaterol- and denopamine-induced dilations were not modified by removal of the endothelium. 5. Pretreatment with L-NG-nitroarginine methyl ester (L-NAME) readily inhibited ACh-induced vasodilations. However, neither procaterol- or denopamine-induced vasodilation was modified by L-NAME treatment. 6. From these results, it is concluded that in the rat common carotid arteries (1) there are abundant beta2- and a few beta1-adrenoceptors, and (2) there is no participation of the endothelium-dependent mechanism in beta-adrenoceptor mediated vasodilations.