ALPHA-ADRENOCEPTOR AND BETA-ADRENOCEPTOR BLOCKING ACTION OF CARVEDILOL IN THE CANINE MESENTERIC-ARTERY AND VEIN

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Abstract
We observed the effects of carvedilol, a novel beta adrenoceptor blocker, on electrical responses of smooth muscle cells produced by endogenous and exogenous norepinephrine (NE) in isolated canine mesenteric artery and vein. Carvedilol inhibited the NE-induced depolarization in the artery but not in vein, with potencies equivalent to prazosin, i.e., carvedilol blocked alpha1 and adrenoceptors in arterial smooth muscles. Stimulation of perivascular nerves evoked an excitatory junction potential (e.j.p.) and a slow depolarization in these vascular smooth muscles. Carvedilol inhibited the slow depolarization evoked in the artery but not in the vein, with no marked inhibition of the e.j.p.s. High concentrations (10-5 M) of carvedilol inhibited the e.j.p., slow depolarization, and also the compound action potentials of sympathetic nerve bundles running along the mesenteric vessels, suggesting that these inhibitions were due to local anesthetic actions. The e.j.p. amplitude was increased by isoprenaline and was decreased by NE and isoprenaline actions were antagonized by yohimbine and propranolol, respectively. Carvedilol inhibited the isoprenaline-actions but not the NE actions on the e.j.p., suggesting that this drug blocked prejunctional beta adrenoceptors but not the alpha2 adrenoceptors. These results indicate that carvedilol blocks alpha1 and beta adrenoceptors but not alpha2 adrenoceptors in vascular tissues.

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