期刊文献+

卡托普利和肾切除对肾性高血压大鼠左室心肌MHC基因转录变化的影响 被引量:1

The Effect of Captopril and Removal of Ischemic Kidney on the Expression of MHC of the Left Ventricle in Hypertensive Rats
下载PDF
导出
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
关键词 卡托普利 肾切除 MHC基因 肾性高血压 心肌肥厚 Captopril removal of ischemic kidney MHC
  • 引文网络
  • 相关文献

参考文献3

二级参考文献1

  • 1陈伟红,生理学报,1995年,47卷,173页

共引文献4

同被引文献27

  • 1冯凯,姚平,徐锦秀.培他乐克、波依定和洛汀新对高血压病左室重构的影响[J].苏州医学院学报,2000,20(10):918-920. 被引量:1
  • 2王玮,李源,崔致贤,黄晨,张珊红,张勇翔.维拉帕米抑制肥厚心肌细胞提取物促心肌细胞生长作用的研究[J].第四军医大学学报,1996,17(3):194-194. 被引量:5
  • 3Vaux DL., Strasser A. The molecular biology of opoptosis.Proc Natl Acad Sci USA, 1996,93:2239
  • 4Bennett MR., Evan GI., Newby AC., et al. Deregulated expression of the-myconcogeneobolishes inhibition of proliferation of rat vascular smooth muscle cells by serum reduction, intefferon-γ, heporin, and cyclic nudeotide analogues and induces apoptosis. Circulation Research,1994,74 (3) :525
  • 5Dariusz L., Yejun Z., Mikko L., et al. Apoptosis of vascular smooth muscle cells. A Pathol, 1994,145 (6):1265
  • 6Dia S. ,Pollack MD. Proto-oncogenes and the cardiovascular system. CHEST, 1995,107 (3) :826
  • 7Oscar H., Bing L. Hypothesis:opoptosis may be a mechani-sm for the transition to heart failture with chronic pressure overload. J Mol cell Cardiol,1994,26:943
  • 8Nagase-Ml. Do angiotention converting enzyme and calcium channel blocker intervene in the progression of renal disease besides by lowering systemic hypertention?Nippon-Rinsho, 1997,55 (8) :2116-2122
  • 9Matsubara,-L-S. Myocardial fibrosis rather than hypertrophy induces diastolic dysfunction inrenovascular hypertensive rats. Can-J-Physiol-Pharmacol, 1997,75(12):1328-1334
  • 10Linz,-W. Long-term ACE inhibition doubles lffespan of hypertensive rats. Circulation, 1997,96 (9):3164-3172

引证文献1

;
使用帮助 返回顶部