Potentiation in various agonists-induced contractions of rabbit mesenteric artery by sulfhydryl reagents.

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Abstract
The role of sulfhydryl and disulfide groups as determinants of rabbit mesenteric arterial responses to various contractile agonists were determined. The addition of 1 .times. 10-3 M or of 1 .times. 10-2 M 2-mercaptoethanol (2-MEt), a sulfhydryl reagent, produced a leftward displacement (potentiation) of the concentration-response curves of mesenteric arterial strips for KCl. Dithiothreitol (DTT), a reagent that reduces disulfide bonds to sulfhydryl groups, also potentiated the contractile response to KCl in this strip. In mesenteric arterial strips treated with 14 mM KCl after exposure to Ca2+-free Krebs'' bicarbonate solutions containing 0.1 mM EGTA [ethylene glycol bis(.beta.-amino-ethyl-ether) N,N,N'',N''-tetraacetic acid], the addition of CaCl2 in a concentration of 2.5 mM caused a contraction (14 mM KCl-induced Ca2+-contraction). The presence of 2-MEt or DTT expectedly potentiated this 14 mM KCl-induced Ca2+-contraction. Verapamil, a Ca2+ antagonist, inhibited the 14 mM KCl-induced Ca2+-contraction both in the presence and the absence of these sulfhydryl reagents. 2-MEt also potentiated the contractile responses of mesenteric arterial strips to histamine, norepinephrine, angiotensin II and prostaglandin F2.alpha., suggesting that the potentiation by the sulfhydryl reagent is a nonspecific effect. This sulfhydryl reagent potentiated each agonist-induced Ca2+-contraction. Evidently reduction of a disulfide bridge to a sulfhydryl group at Ca2+ channels increases transmembrane influx of Ca2+ in strips of rabbit mesenteric artery and the increased Ca2+ influx in turn accompanied the contractile responses to various agonists.

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