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作 者:闫德俊[1] 尹胜[1] 丁圣刚[2] 沈兵[1] 杜鹃[1]
机构地区:[1]安徽医科大学基础医学院生理学教研室,合肥230032 [2]安徽医科大学第一附属医院儿科,合肥230022
出 处:《安徽医科大学学报》2017年第8期1137-1141,共5页Acta Universitatis Medicinalis Anhui
基 金:安徽省高校优秀青年人才支持计划
摘 要:目的探讨钙库操纵钙内流(SOCE)和钠钙交换体(NCX)在卡巴胆碱引起的气管平滑肌收缩中的作用。方法采用小鼠离体气管实验,观察NCX特异性阻断剂KBR7943、电压依赖型钙通道阻断剂尼非地平、Orai1阻断剂BTP2对卡巴胆碱引起的气管收缩的抑制效应。结果 KBR7943和BTP2显著阻断了累积浓度卡巴胆碱引起的小鼠气管收缩和卡巴胆碱引起的SOCE介导的气管收缩,而尼非地平未显著阻断卡巴胆碱引起的气管收缩。结论 NCX和Orai1都参与介导卡巴胆碱引起的气管平滑肌收缩,Orai1主要参与卡巴胆碱引起的起始阶段的瞬时收缩,NCX主要参与后期的持续收缩,而起始阶段的Orai1介导的钙内流可能是激活NCX的前提条件,阻断Orai1的同时也会导致后期NCX引起的收缩阻断,两者共同参与介导卡巴胆碱引起的收缩。Objective To investigate the role of store-operated calcium entry ( SOCE ) and sodium calcium ex-changer ( NCX) in the contraction of tracheal smooth muscle induced by carbachol. Methods Isolated tracheal rings of mice were used to observe the effect of NCX blocker KB-R7943, voltage-dependent calcium channel bloc-ker nifedipine and Orail blocker BTP2 on carbachol-induced tracheal contraction. Results K B - R 7 9 4 3 and B T P 2 were significantly inhibited the cumulative mouse tracheal contraction induced by carbachol and carbachol-induced SOCE-mediated tracheal contraction, whereas nifedipine did not significantly affect carbachol-induced tracheal con-traction. Conclusion Both NCX and Orail contribute carbachol-induced contraction of tracheal smooth muscle. Orail mainly participates in the initial phase of contraction. NCX is mainly involved in the continued contraction of the late phase. Orail -mediated calcium intracellular flow may be a prerequisite for activation of NCX, blocking Orail also led to late NCX-induced contraction blockage and they both are involved in mediating cardbo-induced contractility.
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