Effects of amosulalol on the electrical responses of guinea-pig vascular smooth muscle to adrenoceptor activation.

Abstract

The effects of amosulalol, a newly synthesized sulphonamide-substituted phenylethylamine derivative, on electrical responses of smooth muscle cells of the guinea-pig vascular tissues to noradrenaline, isoprenaline and perivascular nerve stimulation were investigated. Amosulalol (10(-10) -10(-5)M) did not alter the resting membrane potential of smooth muscle cells of the mesenteric artery, the mesenteric vein, the main pulmonary artery and the portal vein. In the mesenteric artery, main pulmonary artery and portal vein, but not in the mesenteric vein, membrane depolarizations produced by noradrenaline were antagonized by amosulalol. In the portal vein, membrane hyperpolarizations produced by isoprenaline were antagonized by amosulalol. In the mesenteric artery, amosulalol (over 10(-6)M) enhanced the amplitude of excitatory junction potentials (e.j.ps) produced by perivascular nerve stimulation. Amosulalol antagonized the noradrenaline-induced decrease in the e.j.p. amplitude; this effect was much weaker than that of phentolamine. Amosulalol also antagonized the isoprenaline-induced enhancement of the e.j.p. amplitude. In the mesenteric vein, the slow depolarizations produced by perivascular nerve stimulation were depressed by amosulalol (over 10(-6)M), but the effect was much weaker than that of prazosin, yohimbine or phentolamine. Actions of amosulalol on electrical properties of vascular tissues can be summarized as follows: amosulalol blocks alpha 1- and beta-adrenoceptors. It also blocks alpha 2-adrenoceptors, though weakly.