Role of Cl- current in endothelin-1-induced contraction in rabbit basilar artery
Role of Cl- current in endothelin-1-induced contraction in rabbit basilar artery
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DOI：
10.1152/ajpheart.2001.281.5.h2159
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发表时间：
2001-11-01
影响因子：
4.8
通讯作者：
Zhang, JH
中科院分区：
文献类型：
--
作者：
Dai, Y;Zhang, JH
Cl-外流引起平滑肌细胞去极化和收缩。本研究旨在探讨Cl-通道在内皮素-1（ET-1）收缩兔基底动脉中的作用。雄性新西兰白色家兔（n=26），体重1.8-2.5 kg，通过过量戊巴比妥实施安乐死。切除基底动脉进行等长张力记录。ET-1在正常Cl- Krebs-Henseleit碳酸氢盐缓冲液（123 mM Cl-）中引起兔基底动脉浓度依赖性收缩。通过以下操作可以减少ET-1诱导的收缩：1）布美他尼抑制Na+-K+-2Cl（-）共转运蛋白（3 × 10-（5）和10（-4）M），2）不含碳酸氢盐的溶液，以禁用Cl-/HCO 3-交换器，和3）与Cl-通道阻断剂尼氟灭酸，5-硝基-2-甲基-苯甲酸（5-nitro-2-hydroxyethanol）（3-苯基丙基氨基）苯甲酸和茚满基氧基乙酸94。用甲磺酸（113 mM）取代细胞外Cl-（10 mM）可增强ET-1诱导的收缩。Cl-通道参与ET-1引起的兔基底动脉收缩。
Cl- efflux induces depolarization and contraction of smooth muscle cells. This study was undertaken to explore the role of Cl- channels in endothelin-1 (ET-1)-induced contraction in rabbit basilar artery. Male New Zealand White rabbits (n=26), weighing 1.8-2.5 kg, were euthanized by an overdose of pentobarbital. The basilar arteries were removed for isometric tension recording. ET-1 produced a concentration-dependent contraction of the rabbit basilar artery in the normal Cl- Krebs-Henseleit bicarbonate buffer (123 mM Cl-). The ET-1-induced contraction was reduced by the following manipulations: 1) inhibition of Na+-K+-2Cl(-) cotransporter with bumetanide (3 x 10-(5) and 10(-4) M), 2) bicarbonate- free solution to disable Cl-/HCO3- exchanger, and 3) preincubation of rings with the Cl- channel blockers niflumic acid, 5-nitro-2-(3-phenylpropylamino) benzoic acid, and indanyloxyacetic acid 94. The ET-1-induced contraction was enhanced by substitution of extracellular Cl- (10 mM) with methanesulfonic acid (113 mM). Cl- channels are involved in ET-1-induced contraction in the rabbit basilar artery.