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目的 探讨肌浆网Ca2+释放通道在原发性高血压发病机制中的变化特点。方法 提取2、4、6、8、10、12周龄各组雄性自发性高血压大鼠(spontaneously hypertensive rats,SHR)和正常血压大鼠(Wistar-kyoto rats,WKY)心室肌、血管平滑肌、肝脏和肾脏组织的总RNA,共294个样品,利用高通量RNA阵列技术检测肌浆网兰尼碱受体2(ryanodine receptor,RyR2)和1,4,5-三磷酸肌醇受体1(inositol 1,4,5-triphosphate receptors,IP3R1)在不同周龄SHR中mRNA的表达谱改变。结果 与同周龄WKY相比较,SHR在6、8、10、12周龄血压出现显著性升高(P均<0.01),10、12周龄心室肌重量/体重比出现显著增加(P均<0.01),心肌中RyR2基因表达在4、6、8、10、12周龄出现显著性升高(P<0.05或P<0.01),IP3R1基因表达在6、8、10、12周龄出现显著性升高(P<0.05或P<0.01)。血管平滑肌组织中RyR2基因表达在4、6、8、10、12周龄出现显著性升高(P<0.05),IP3R1基因表达在4、6、8、10、12周龄出现显著性升高(P<0.05或P<0.01)。肝脏和肾脏组织中未见上述基因的明显表达。结论 肌浆网Ca2+释放通道受体蛋白RyR2和IP3R1 mRNA表达变化是实验性高血压发生和发展过程中重要的分子生物学机制。
Objective To investigate the changes of sarcoplasmic reticulum Ca2 + release channel in the pathogenesis of essential hypertension. Methods The cardiac hypertrophy was induced in spontaneously hypertensive rats (SHR) and normal Wistar rats (WKY) at 2, 4, 6, 8, Total RNA was extracted from liver, liver and kidney using a total of 294 samples. The ryanodine receptor 2 (RyR2) and inositol 1,4,5-triphosphate receptor 1 (inositol 1,4,5-triphosphate receptors, IP3R1) in different age SHR mRNA expression profile changes. Results Compared with WKY at the same week, SHR at 6, 8, 10 and 12 weeks of age significantly increased (P <0.01), and the weight / weight ratio of ventricular muscle increased significantly at 10 and 12 weeks <0.01). The expression of RyR2 gene in myocardium was significantly increased at 4,6,8,10,12 weeks (P <0.05 or P <0.01), and the expression of IP3R1 gene at 6,8,10,12 weeks Significantly increased (P <0.05 or P <0.01). The expression of RyR2 gene in vascular smooth muscle tissue was significantly increased at 4,6,8,10,12 weeks (P <0.05), and the expression of IP3R1 gene was significantly increased at 4,6,8,10,12 weeks (P <0.05 or P <0.01). No obvious expression of the above genes was found in liver and kidney tissues. Conclusion The changes of RyR2 and IP3R1 mRNA expression in the sarcoplasmic reticulum Ca2 + release channel receptor are important molecular mechanisms in the pathogenesis and development of hypertension.