大鼠尾加压素II收缩大鼠肺动脉干与蛋白激酶C通路相关性研究  

作　　者：薛必成[1] 陈少贤[1] 龚永生[2] 徐正衸[3] 王良兴[1] 范小芳[2] 

机构地区：[1]温州医学院附属第一医院,325000 [2]温州医学院肺心病研究室 [3]温州医学院病理生理学教研室

出　　处：《浙江临床医学》2007年第1期3-4,共2页Zhejiang Clinical Medical Journal

基　　金：浙江省教育厅 科学基金20020468号

摘　　要：目的研究大鼠尾加压素-Ⅱ（RUII）收缩大鼠离体肺动脉干环与细胞信号转导通路蛋白激酶C通道的关系。方法从雄性Sprague—Dauley大鼠中分离出肺动脉干，切成3—4mm的血管环，用RUII（10nmol／L）预收缩血管达坪台期后，加入蛋白激酶C通道阻断剂H-7，制备H-7（0．1-100μmol／L）浓度一效应舒张曲线，最后分别计算EC50和Emax。结果H-7呈浓度依赖性舒张大鼠RUII预收缩的肺动脉干-log[EC50]=5．26±0．36，Emax=（97．21±17．86）％。结论细胞信号转导通路蛋白激酶C通道的激活参与大鼠尾加压素-Ⅱ收缩大鼠肺动脉干效应。Objective The aim of our study was to investigate the influence of protein kianse C inhibition on rat urotensin Ⅱ induced vasoconstriction. Methods The train mmeus pulmanalis was dissected from the nude Sprague - Dawley rat, artery ring width was 3 - 4mm. Inhibitor of protein kinase C channel, H- 7（0.1 - 100/μmol/L） were added into medium after rat urotensin Ⅱ（ 10nmol/L）indueed vasoconstriction had reached plateau to construct the relaxant concentration- response curves and their EC50 and Emax. Results H - 7 caused concentration - dependent relaxations of rat urotensin Ⅱ preeontracted arteries [ - log[EC50] = 5.26 ± 0.36. Emax = （97.21 ± 17.86）% of the response to 10 nmoL/L rat urotensin Ⅱ]. Conclusion Rat UII induced rat main pulmonary artery contraction is related to the activation of protein kinase C signal transduciton pathway.

关 键 词：尾加压素-Ⅱ 蛋白激酶C 肺动脉干 

分 类 号：R341[医药卫生—基础医学]