Ca^(2+)激活Cl^-通道参与去甲肾上腺素诱发的大鼠尾动脉收缩反应  

Ca^(2+)-activated Cl^- channels contribute to norepinphrine-induced contraction of rat tail artery

作　　者：王贞[1] 柴强[2] 刘志向[2] 刘德祥[3] 陈连璧[1] 

机构地区：[1]山东大学医学院生理学研究所,山东济南250012 [2]山东省医学科学院生理室,山东济南250062 [3]山东大学医学院医学心理学研究所,山东济南250012

出　　处：《山东大学学报（医学版）》2005年第4期277-279,共3页Journal of Shandong University:Health Sciences

基　　金：山东省卫生系统九五攻关项目[鲁卫科教字(1997)第9号]

摘　　要：目的:观察Ca^(2+)激活Cl^-通道是否参与去甲肾上腺素(NE)诱发的大鼠尾动脉平滑肌收缩反应。方法:记录大鼠尾动脉肌条的等长收缩,观察不同药物对NE的收缩影响。结果:①硝呋咪酸(NFA)和维拉帕米(Vera)可显著抑制NE诱发的血管条收缩反应,且硝呋咪酸具有浓度依赖性。同时给予NFA及Vera时两者对NE诱发的血管条收缩的抑制作用相迭加;②用低氯缓冲液代替PSS液灌流标本以增强Cl-通道活性时,尾动脉条对NE的收缩反应明显增强,此反应仍可被NFA所抑制。结论:Ca2+激活的Cl-通道参与NE诱发的大鼠尾动脉平滑肌收缩反应。Objective: To observe whether Ca2+-activated Cl- channels play a role in norepinphrine (NE)-induced contraction of rat tail artery. Methods: The tail artery was isolated from the anesthetized Wistar rats. Under a dissecting microscope the artery was cut helically into strip and then mounted vertically on a stainless steel holder in an organ chamber containing PSS aerated with a mixture of 95% O2-5% CO2. The isometric contraction was recorded. The contractile reactivity of the vessel strip to different chemicals was expressed as a percentage of 100 mmol/L KCl-induced contraction of the same strip. Results: ①The Cl- channel blocker-niflumic acid (NFA) produced a dose-dependent inhibitory effect on NE-induced contraction of the rat tail artery strip. The Ca2+ channel blocker-Verapamil (Vera) had an inhibitory effect on NE-induced contraction of the artery strip. The inhibitory effects of NFA and Vera were additive and coordinated. ② Decreasing the extracellular Cl- concentration increased the contractile response to NE significantly,which was still inhibited by NFA. Conclusion: The Ca2+-activated chloride channel activity contributes to NE-induced contraction of the rat tail artery.

关 键 词：Ca^2+激活Cl^-通道 去甲肾上腺素 硝呋咪酸 尾动脉 大鼠 Wistar 

分 类 号：R331.32[医药卫生—人体生理学]