摘要
用二肾一夹(2KIC)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)2KIC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)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)在术后第4周给予血管紧张素转换酶抑制剂卡托普利和术后第8周切除肾动脉狭窄侧肾脏可使2KIC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β-NHC基因表达增强。这些结果提示在2K1C肾性高血压中,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2KIC肾性高血压过程中的心肌肥厚和MHC基因表型的转移。
The expression of myosin heavy chain isogene of the left ventricle was investigated in two-kidney, one-clip renal hypertensive rats. The results showed as follows: (1) As blood pressure increaed, left ventricle became hypertrophy, α-MHC mRNA expression was reduced and β-MHC mRNA expression was increased in 2K1C renal hypertensive rats.(2) After treating with captopril and removal of the ischemic kidney, blood pressure reduced, left ventricular hypertrophy regressed, the increase in α-MHC mRNA expression and reduction in β-MHC mRNA expression were inhibited. These results suggested that left ventricular hypertrophy and the MHC isoform transitions may be induced by pressure overload. Captopril and removal of ischemic kidney prevented hypertension, ventricular hypertrophy and MHC isoform transition.
出处
《暨南大学学报(自然科学与医学版)》
CAS
CSCD
1998年第2期13-17,共5页
Journal of Jinan University(Natural Science & Medicine Edition)
基金
美国中华医学基金会
国家自然科学基金