【摘要】 目的观察尾加压素Ⅱ(U-Ⅱ)对不同血压水平的自发性高血压大鼠(SHR)胸主动脉的收缩效应和U-Ⅱ对血管平滑肌细胞(VSMC)内ERK1/2和p38MAPK磷酸化的影响,以进一步明确U-Ⅱ对SHR的血管效应及其可能机制。方法离体血管灌流实验测定U-Ⅱ对胸主动脉张力的影响,采用免疫荧光标记UT受体在VSMC的表达,并通过蛋白质印迹的方法观察U-Ⅱ对VSMC内ERK1/2和p38MAPK磷酸化的作用。结果U-Ⅱ受体分布在VSMC上,累积浓度的U-Ⅱ对成年SHR去除内皮的胸主动脉环收缩效应明显强于WKY大鼠;在VSMC细胞内,U-Ⅱ可以浓度依赖性地激活VSMC内ERK1/2磷酸化,但对p38MAPK没有作用;ERK1/2阻断剂的应用不能阻断(肌凝蛋白轻链)MLC的磷酸化。结论U-Ⅱ对SHR离体血管表现出较强的收缩作用,可能通过ERK1/2及p38MAPK以外的其他通路参与了MLC的磷酸化以及VSMC的收缩效应。更多还原

【Abstract】 Objective To observe the vasoconstrictor effect of urotensin Ⅱ （U-Ⅱ） on thoracic aorta of spontaneously hypertensive rats （SHR） and the effects of U-Ⅱ on ERK_1/2 and p38 MAPK phosphorylation in cultured vascular smooth muscle cells （VSMC）. Methods Isolated thoracic aorta organ bath study was used to observe the vasoconstrictor effect of U-Ⅱ. The phosphorylation levels of ERK_1/2 and p38MAPK were detected by Western blot. Results We observed that U-Ⅱ elicited a greater contractile response in endothelium-denuded thoracic aorta of SHR than that of the WKY rats. U-Ⅱ caused a dose-dependent ERK_1/2 phosphorylation,which was blocked by ERK_1/2 inhibitors. While the MLC phosphorylation was not prevented by ERK_1/2 inhibitors. Conclusions ERK_1/2 or p38MAPK was not the passageway through which U-Ⅱ was involved in the greater vasoconstriction in SHR.更多还原