【摘要】 实验用二肾一夹（2K1C）肾性高血压大鼠模型，探讨心肌肥厚发生和逆转以及肌球蛋白重链（myosinheavychain，MHC）基因表达的改变。结果表明：（1）2K1C肾性高血压大鼠术后第2～12周，动脉血压持续升高；左室重量／体重（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。（2）术后第4周给予血管紧张素转换酶抑制剂、巯甲丙脯酸和术后第8周切除肾动脉狭窄侧肾脏可使2K1C肾性高血压大鼠动脉血压下降；左心室肥厚发生逆转；抑制左心室α-MHC基因表达减弱和抑制β-MHC基因表达增强。这些结果提示在2K1C肾性高血压过程中，动脉血压升高是左心室肥厚、左心室肌球蛋白MHC基因表型转换的重要因素；肾素-血管紧张素系统可能参与2K1C肾性高血压过程中的心肌肥厚和MHC基因表型的转换。更多还原

【Abstract】 The changes in the expression of cardiac α- and β-myosin heavy chain (MHC)gene of the left ventricle were investigated in two-kidney, one-clip (2K1C) renal hypertensive rats. The results were as follows: (1) When blood pressure was increased,the left ventricle became hypertrophic, α-MHC gene expression was reduced and β-MHC gene expression was increased in ZK1C renal hypertensive rats. (2) When the animal was treated with captopril, angiotensin converting enzyme inhibitor 4 W after operation and then 8 W with removal of the ischemic kidney, the blood pressure was decreased with attendant regression of left ventricular hypertrophy, while the increase inβ-MHC mRNA level was attenuated and the inhibition of α-MHC mRNA level was reduced. The above results suggest that the rise in arteral pressure is an important factorin the left ventricular hypertrophy and the MHC gene switch. Renin angiotension system may be involved in the cardiac hypertrophic and MHC gene switch during the development and maintenance of ZK1C renal hypertension.更多还原