动脉血压在肾性高血压大鼠心肌α-和β肌球蛋白重链基因表达中的作用

本实验用肾性高血压大鼠模型,探讨动脉血压在心肌肥厚和肌球蛋白重链(Myosinheavy chain,MHC)基因表达中的作用.结果表明:(1)二肾二夹(2K1C)肾性高血压大鼠,术后48～72h,血压升高.α-MHC基因表达减弱,β-MHC基因表达增强,左室重量/体重(LVW/BW)比值变化不明显;(2)二肾一夹(2K1C)肾性高血压大鼠术后第2～12w,动脉血压持续升高,LVW/BW比值明显升高,左心室α-MHC基因表达明显减弱,β-MHC基因表达明显增强;(3)血管紧张素转换酶抑制剂、巯甲丙脯酸可使2K1C肾性高血压大鼠动脉血压下降,左室肥厚发生逆转,抑制左心室α-MHC基因表达减弱和β-MHC基因表达增强.这些结果提示,在肾性高血压过程中,动脉血压升高是左心室肥厚、左室心肌MHC基因转换(switch)的重要因素,肾素-血管紧张素系统可能参与肾性高血压过程中的心肌肥厚和MHC基因转换.

The role of arterial blood pressure in changes in the expression of a-and β-myosin heavy chain gene of cardiac myocardium in renal hyper

The changes in the expression of cardiacα-and β-myosin heavy chain (MHO gene of the left ventricle were investigated in renal hypertensive rats. These results showed as follows:1. The increase in blood pressure, the reduction in α-MHC gene expression and the increase in β-MHC gene expression and no change in LVW/BW were observed at 48-72h after constriction of bilateral renal arteries in 2K2C renal hypertensive rats. 2. As blood pressure increased, left ventricle became hypertrophy, α-MHC gene expression was reduced and β-MHC gene expression was increased in 2K1C renal hypertensive rats. 3. After treating with captopril, an angiotensin converting enzyme inhibitor, blood pressure was reduced, the left ventricular hypertrophy was regressed, the increase in β-MHC mRNA level and reduction in α-MHC mRNA level were inhibited. The results suggest that the rise in arterial pressure is the important factor in the left ventricular hypertrophy and the MHC gene swtich. RAS may involve in the cardiac hypertrophy and MHC gene switch during the development and maintenance of renal hypertension.