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首页> 外文期刊>American Journal of Physiology >Role of Cl- current in endothelin-1-induced contraction in rabbit basilar artery.
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Role of Cl- current in endothelin-1-induced contraction in rabbit basilar artery.

机译:Cl-电流在内皮素-1诱导的兔基底动脉收缩中的作用。

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摘要

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-/HCO 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.
机译:Cl-流出引起平滑肌细胞的去极化和收缩。进行这项研究以探讨Cl通道在内皮素1(ET-1)诱导的兔基底动脉收缩中的作用。体重超过1.8-2.5公斤的雄性新西兰白兔(n = 26)被过量的戊巴比妥安乐死。取出基底动脉以记录等距张力。 ET-1在正常的Cl-Krebs-Henseleit碳酸氢盐缓冲液(123 mM Cl-)中产生兔基底动脉的浓度依赖性收缩。通过以下操作减少了ET-1诱导的收缩:1)用布美他尼(3 x 10(-5)和10(-4)M)抑制Na + -K + -2Cl-共转运蛋白,2)不含碳酸氢盐的溶液禁用Cl- / HCO交换剂,以及3)用Cl-通道阻滞剂尼氟酸,5-硝基-2-(3-苯基丙基氨基)苯甲酸和茚满基氧乙酸94预孵育环。ET-1诱导的收缩为通过用甲磺酸(113 mM)取代细胞外Cl-(10 mM)来增强。 Cl-通道参与ET-1诱导的兔基底动脉的收缩。

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