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首页> 外文期刊>Japanese Journal of Pharmacology >POTENTIATION IN VARIOUS AGONISTS-INDUCED CONTRACTIONS OF RABBIT MESENTERIC ARTERY BY SULFHYDRYL REAGENTS
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POTENTIATION IN VARIOUS AGONISTS-INDUCED CONTRACTIONS OF RABBIT MESENTERIC ARTERY BY SULFHYDRYL REAGENTS

机译:巯基试剂在各种激动剂诱导的兔中肠动脉收缩中的增强作用

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References(28) Cited-By(3) The role of sulfhydryl and disulfide groups as determinants of rabbit mesenteric arterial responses to various contractile agonists were determined. The addition of 1×10-3 M or of 1×10-2 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 Ca2+-free Krebs' bicarbonate solutions containing 0.1 mM EGTA, 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 KCI-induced Ca2+-contraction. Verapamil, a calcium antagonist, inhibited the 14 mM KCI-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 F2α suggesting that the potentiation by the sulfhydryl reagent is a nonspecific effect. This sulfhydryl reagent potentiated the each agonist-induced Ca2+-contraction. It is concluded that 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.
机译:参考文献(28)被引用的By(3)确定了巯基和二硫基作为兔肠系膜动脉对各种收缩激动剂反应的决定因素。添加1×10-3 M或1×10-2 M 2-巯基乙醇(2-M Et)(巯基试剂)会导致KCl肠系膜动脉条的浓度-响应曲线向左移动(增强) 。二硫苏糖醇(DTT)是一种还原二硫键与巯基的试剂,在该试纸条中也增强了对KCl的收缩反应。在暴露于含有0.1 mM EGTA的不含Ca2 +的克雷布斯碳酸氢盐溶液中后,用14 mM KCl处理的肠系膜动脉条中,添加浓度为2.5 mM的CaCl2引起收缩(14 mM KCl诱导的Ca2 +收缩)。 2-MEt或DTT的存在有望增强这种14 mM KCI诱导的Ca2 +收缩。钙拮抗剂维拉帕米在存在和不存在这些巯基试剂的情况下均抑制14 mM KCI诱导的Ca2 +收缩。 2-MEt还增强了肠系膜动脉条对组胺,去甲肾上腺素,血管紧张素II和前列腺素F2α的收缩反应,表明巯基试剂的增强作用是非特异性的。该巯基试剂增强了每个激动剂诱导的Ca2 +收缩。结论是,在Ca2 +通道上的二硫键还原成巯基会增加兔肠系膜动脉条中Ca2 +的跨膜流入,而增加的Ca2 +流入又伴随着对各种激动剂的收缩反应。

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