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

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Abstract
1 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. 2 Amosulalol (10−10−10−5m) 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. 3 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. 4 In the portal vein, membrane hyperpolarizations produced by isoprenaline were antagonized by amosulalol. 5 In the mesenteric artery, amosulalol (over 10−6m) enhanced the amplitude of excitatory junction potentials (e.j.ps) produced by perivascular nerve stimulation. 6 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. 7 In the mesenteric vein, the slow depolarizations produced by perivascular nerve stimulation were depressed by amosulalol (over 10−6m), but the effect was much weaker than that of prazosin, yohimbine or phentolamine. 8 Actions of amosulalol on electrical properties of vascular tissues can be summarized as follows: amosulalol blocks α1- and β-adrenoceptors. It also blocks α2-adrenoceptors, though weakly.

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