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目的探讨高血压血管平滑肌细胞增生和ERK激活的机制。方法采用免疫组织化学和Westernblotting技术,对比观察肾血管性高血压和自发性高血压大鼠肾细小动脉平滑肌细胞中磷酸化细胞外信号调节激酶1/2(ERK1/2)和P21ras表达。结果实验期间,Wistar肾血管性高血压组动脉血压从(104±18)mmHg升高到实验结束时的(198±33)mmHg,自发性高血压大鼠16周龄时的血压为(163±23)mmHg。肾血管性高血压组肾小球发生了明显的纤维化(P<0.05),自发性高血压大鼠肾小球纤维化等与对照组无显著性差异。肾血管性高血压组入球动脉、小叶间动脉、叶间动脉和弓形动脉血管平滑肌细胞中磷酸化ERK1/2染色阳性率分别为7.09%、14.57%、29.44%和13.63%,均明显高于对照组(P<0.01)。自发性高血压大鼠入球动脉、小叶间动脉、叶间动脉和弓形动脉血管平滑肌细胞中磷酸化ERK1/2染色阳性率分别为16.09%、24.17%、32.44%和18.61%,均明显高于对照组(P<0.01);肾血管性高血压组和16周龄自发性高血压大鼠入球动脉、小叶间动脉和弓形动脉平滑肌细胞中P21ras的阳性率明显高于对照组(P<0.01);Westernbloting检测可见高血压组和16周龄自发性高血压大鼠肾组织磷酸化ERK1/2和P21ras蛋白含量明显高于对照组(P<0.01)。结论在大鼠两肾一夹型高血压和自发性高血压时,P21ras基因表达增加使部分血管平滑肌细胞丝裂原激活蛋白激酶系统激活,导致部分小动脉血管平滑肌细胞增生。
Objective To investigate the mechanism of hypertensive vascular smooth muscle cell proliferation and ERK activation. Methods Immunohistochemistry and Western blotting were used to observe the expressions of phosphorylated ERK1 / 2 and P21ras in renal arteriolar hypertensive rats and spontaneously hypertensive rats. Results During the experiment, arterial blood pressure in Wistar renovascular hypertension increased from (104 ± 18) mmHg to (198 ± 33) mmHg at the end of the experiment, and blood pressure at 16 weeks of spontaneous hypertensive rats was (163 ± 23) mmHg. Renal vascular hypertensive group glomerular fibrosis (P <0.05), spontaneous hypertensive rats with glomerular fibrosis and the control group no significant difference. The positive rate of phosphorylated ERK1 / 2 staining in arteries, interlobular arteries, interlobar arteries and arcuate arterial smooth muscle cells of renovascular hypertension group were 7.09%, 14.57%, 29.44% and 13.63%, respectively, which were significantly higher than those of Control group (P <0.01). The positive rates of phosphorylated ERK1 / 2 staining in spontaneous hypertensive rats were 16.09%, 24.17%, 32.44% and 18.61% respectively, which were significantly higher than those in the afferent arteries, interlobular arteries, interlobar arteries and arcuate arterial smooth muscle cells (P <0.01). The positive rate of P21ras in the intima-media, interlobular arteries and arcuate arterial smooth muscle cells in the renovascular hypertension group and 16-week-old spontaneous hypertensive rats was significantly higher than that in the control group (P <0.01) Western blotting showed that the levels of phosphorylated ERK1 / 2 and P21ras in renal tissue of hypertensive rats and 16-week-old spontaneously hypertensive rats were significantly higher than those of the control group (P <0.01). Conclusion The increase of P21ras gene activates the mitogen-activated protein kinase system of some vascular smooth muscle cells and leads to the proliferation of some arteriolar smooth muscle cells in rats with two-kidney-one hypertension and spontaneous hypertension.