硝苯地平对氯化钾、去甲肾上腺素及内皮素诱导离体大鼠血管收缩的影响  

Effect of nifedipine on vasoconstriction induced by KCl,norepinephrine and endotheine-1 in vitro rats

作　　者：杜珍[1] 谢学渊[1] 张沂[1] 

机构地区：[1]海军总医院药剂科,北京100048

出　　处：《海军医学杂志》2013年第1期25-28,共4页Journal of Navy Medicine

摘　　要：目的观察硝苯地平对KCl、去甲肾上腺素(NE)、内皮素(ET-1)诱导离体大鼠主动脉血管收缩的影响,并探讨其作用机制。方法以KCl、NE、ET-1在含钙离子和不含钙离子的K-H液中预收缩离体大鼠主动脉环,并观察硝苯地平的收缩血管作用。结果在含钙离子K-H液中,硝苯地平对KCl、NE、ET-1引起的离体大鼠血管收缩作用的半数有效剂量EC50分别为0.072、5.34、0.15μmol/L;在无钙离子K-H液中,硝苯地平对离体大鼠未产生收缩血管作用。结论硝苯地平的扩血管作用与其选择性阻断电压依赖性钙通道有关。Objective To observe the effect of nifedipine on vasoconstriction induced by KCl, norepinephrine （NE） and endotheine-1 （ ET-1 ） in vitro rats and also to probe the mechanisms involved. Methods The aortic rings of in vitro rats were first constricted with KC1, NE and ET-1 in the calciferous and calcium-free Krebs-Henseleit （K-H） solutions, and also to observe the effect of nifedipine on vasodilatation. Results In the calciferous K-H solution, the EC50 values of nifedipine to counteract vasoconstriction induced by KCl, NE and ET-1 were 0. 072, 5.34 and 0.15 μmol/L respectively. In the calcium-free K-H solution, nifedipine failed to produce the expected vasoconstriction. Conclusion The effect of nifedipine on vasoconstriction was closely correlated with the selective blocking of potential-dependent Ca^2 ＋ influx.

关 键 词：硝苯地平 去甲肾上腺素 内皮素 钙通道拮抗剂 

分 类 号：R972.4[医药卫生—药品]