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

• Published in: British journal of pharmacology Vol. 84; no. 2; pp. 489 - 497
• Main Authors: Fujioka, Masahiko, Suzuki, Hikaru
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.02.1985; Nature Publishing; Nature Publishing Group
• Subjects: Animals; Antihypertensive agents; Biological and medical sciences; Cardiovascular system; Electrophysiology; Ethanolamines - pharmacology; Female; Guinea Pigs; In Vitro Techniques; Isoproterenol - pharmacology; Male; Medical sciences; Membrane Potentials - drug effects; Mesenteric Arteries - drug effects; Mesenteric Veins - drug effects; Motor Endplate - drug effects; Muscle, Smooth, Vascular - drug effects; Norepinephrine - pharmacology; Pharmacology. Drug treatments; Phentolamine - pharmacology; Portal Vein - drug effects; Prazosin - pharmacology; Receptors, Adrenergic - drug effects; Sympatholytics - pharmacology; Yohimbine - pharmacology; Rodentia; Smooth muscle; Α2-Adrenergic receptor; Catecholamine; Β-Adrenergic receptor; Vertebrata; Mammalia; Guinea pig; Animal; Blood vessel; Α1-Adrenergic receptor; Antihypertensive agent; Mechanism of action
• ISSN: 0007-1188; 1476-5381
• DOI: 10.1111/j.1476-5381.1985.tb12933.x

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.