压力负荷增加大鼠模型左室心肌血管紧张素Ⅱ-1型受体mRNA及其受体蛋白的改变

Changes of the expression of left ventricular myocardial angiotensin Ⅱ receptor type 1 mRNA and protein in rat with pressure overload

目的:观察压力负荷增加大鼠左室心肌血管紧张素Ⅱ-1型(AT1)受体mRNA及其受体蛋白的表达,探讨压力负荷增加大鼠左室重构的机制。方法:SD大鼠随机分为假手术组和模型组,利用腹主动脉缩窄法制备压力负荷增加大鼠模型,造模8周后观察左室重量指数、左室心肌细胞超微结构的改变;采用RT-PCR的方法检测心肌组织AT1 mRNA表达,采用免疫组织化学染色方法观察心肌组织AT1受体蛋白的改变。结果:与假手术组比较,模型组LVMI(‰)明显增加(P<0.01),左室心肌亚细胞发生改变,左室心肌组织AT1 mRNA表达水平模型组较假手术组升高(P<0.01),左室心肌组织AT1受体蛋白较假手术组上升(P<0.01)。结论:压力负荷增加大鼠在造模8周已形成左室肥厚的病理生理改变,这种左室肥厚的改变可能与左室心肌AT1基因转录与翻译水平均有关。

Objective To observe the expressions of left ventricular myocardial angiotensin （Ang） Ⅱ type 1 （ATI） receptor mRNA and protein in rat with pressure overload, and to investigate the mechanism of left ventricular remodeling under pressure overload. Methods Rat models were constructed by placing a silver clip with internal diameter of 0.7 mm around the abdominal aorta above the renal arteries, then 24 SD male rats were randomly divided into sham operation group and model group. The changes of myocardial hypertrophy [left ventrieular mass index （LVMI） ,left ventricular myocytes ultramicrostructure]was observed after 8 weeks. RT-PCR was used to detect the expression of left ventricular myocardial AT1 receptor mRNA, the change of myocardial AT1 receptor protein was observed by immunohistochemistry. Results LVMI in model group was significantly higher than that in sham operation group （P 〈 0.01 ）. Left ventricular myoeytes ultramierostructure showed cardioeyte hypertrophy in heart tissue in the model group. The expressions of AT1 receptor mRNA and protein in left ventricular myocardial tissue in model group were significantly higher than those in sham operation group （P 〈 0.01）. Conclusion The main physiopathologic changes of left ventricular remodeling were formed in the rat with pressure overload by abdominal aortic constriction after 8 weeks. The mechanism of left ventricular remodeling might be related to the expressions of AT1 receptor mRNA and protein in left ventricular myocardial tissue.