大鼠尾加压素Ⅱ收缩大鼠离体肺主动脉环与MAPK相关

目的:研究大鼠尾加压素II(U-II)对大鼠离体肺主动脉环的收缩效应及与细胞信号转导通路丝裂素活化蛋白激酶(MAPK)的关系。方法:从雄性Sprague-Dauley大鼠中分离出肺主动脉, 切成3-4 mm的血管环, 制备大鼠U-II(0.03-30 nmol/L)的浓度-效应收缩曲线, 另外, 用大鼠U-II(30 nmol/L)预收缩血管达平台期后, 加入MAPK阻断剂PD 98059, 制备PD 98059(0.1 μmol/L-10 μmol/L) 浓度-效应舒张曲线, 最后分别计算EC₅₀和E_max。结果:大鼠U-II是大鼠离体肺主动脉环的有效血管收缩剂EC₅₀=7.95±0.40, E_max=(14.28±6.34)%, 以60 mmol KCl的收缩幅度为100%];PD 98059呈浓度依赖性舒张大鼠U-II预收缩的动脉EC₅₀=5.91±0.45, E_max=(81.39±13.65)%]。结论：大鼠尾加压素II是大鼠肺主动脉有效的血管收缩剂, 细胞信号转导通路MAPK的激活参与其收缩效应。

Rat urotensin-II-induced main pulmonary artery contractions are mediated by MAPK

AIM:To investigate rat Urotensin-II(rat U-II)-induced vasoconstriction of rat main pulmonary arteries and the role of mitogen-activated protein kinase(MAPK). METHODS: The main pulmonary artery was dissected from the male Sprague-Dawley rats and artery ring width was 3-4 mm. Concentration-response curves were generated to rat U-II(0.03 nmol/L-30 nmol/L).Inhibitor of MAPK,PD 98059(0.1 μmol/L-10 μmol/L) were added into the medium after rat U-II(30 nmol/L)induced vasoconstriction had reached plateau to construct the relaxant concentration-response curves and their EC50 and Emax. RESULTS:Rat U-II was a potent vasoconstrictor of isolated rat main pulmonary arteries EC50=7.95±0.40, Emax=(14.28±6.34)% of the response to 60 mmol/L KCl]; PD 98059 caused concentration-dependent relaxations of rat U-II precontracted arteries EC50=5.91±0.45, Emax =(81.39±13.65)%]. CONCLUSION: Rat U-II was a potent vasoconstrictor of rat main pulmonary arteries and this response was mediated through MAPK.