POTENTIATION IN VARIOUS AGONISTS-INDUCED CONTRACTIONS OF RABBIT MESENTERIC ARTERY BY SULFHYDRYL REAGENTS
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概要
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The role of sulfhydryl and disulfide groups as determinants of rabbit mesenteric arterial responses to various contractile agonists were determined. The addition of 1×10<SUP>-3</SUP> M or of 1×10<SUP>-2</SUP> M 2-mercaptoethanol (2-M Et), 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 Ca<SUP>2+</SUP>-free Krebs bicarbonate solutions containing 0.1 mM EGTA, the addition of CaCl<SUB>2</SUB> in a concentration of 2.5 mM caused a contraction (14 mM KCl-induced Ca<SUP>2+</SUP>-contraction). The presence of 2-MEt or DTT expectedly potentiated this 14 mM KCI-induced Ca<SUP>2+</SUP>-contraction. Verapamil, a calcium antagonist, inhibited the 14 mM KCI-induced Ca<SUP>2+</SUP>-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 F<SUB>2α</SUB> suggesting that the potentiation by the sulfhydryl reagent is a nonspecific effect. This sulfhydryl reagent potentiated the each agonist-induced Ca<SUP>2+</SUP>-contraction. It is concluded that reduction of a disulfide bridge to a sulfhydryl group at Ca<SUP>2+</SUP>-channels increases transmembrane influx of Ca<SUP>2+</SUP> in strips of rabbit mesenteric artery and the increased Ca<SUP>2+</SUP> influx in turn accompanied the contractile responses to various agonists.
- 社団法人 日本薬理学会の論文
著者
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Asano Masahisa
Department Of Pharmacology Nagoya City University Medical School
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Hidaka Hiroyoshi
Department Of Pharmacology Nagoya University School Of Medicine
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Hidaka Hiroyoshi
Department Of Pharmacology Mie University
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HIDAKA Hiroyoshi
Department of Biochemistry, Institute for Developmental Research, Aichi Prefecture Colony
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Asano Masahisa
Department of Pharmacolgy, Nagoya City University Medical School
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