肾性高血压大鼠肥大心肌bFGF与丝裂素活化蛋白激酶的表达及氯沙坦对其影响

目的:观察肾性高血压大鼠肥大心肌碱性成纤维细胞生长因子(bFGF)与丝裂素活化蛋白激酶(MAPK)表达的影响以及氯沙坦逆转心肌肥大的作用。方法:制备二肾一夹高血压大鼠模型为实验组,采用氯沙坦作为治疗组,以未进行二肾一夹大鼠作为假手术组,观察3组大鼠术后8周心肌肥大指数、心肌血管紧张素含量、心肌组织bFGF与MAPK的表达。结果:与假手术组相比,实验组大鼠术后8周心肌肥大指数、心肌Ang水平明显增高(分别P<0.01,P<0.05);治疗组大鼠心肌肥大指数则无明显差异,心肌Ang仍保持在高水平。与假手术组相比,实验组心肌bFGF与MAPK表达显著增强(分别P<0.05),而氯沙坦可以显著抑制bFGF与MAPK表达。结论:bFGF、MAPK参与肾性高血压心肌肥大的发生机制,氯沙坦除了阻断Ang诱导的肥大信号转导外,还可能通过抑制bFGF诱导的细胞信号转导途径逆转心肌肥大。

Effects of bFGF,MAPK and losartan on myocardial hypertrophy in renal hypertensive rats

Objective:To determine the effects of myocardial basicfibroblast growth factor(bFGF),mitogen-activated protern kinase(MAPK)and Losartan onmyocardial hypertrophy in hypertensive rats.Methods:Renal hypertension was made by two kidney one clip as experiment group,the rats were treated by losartan as treatment group,the rats were not operated as sham group.The blood pressure,cardiac hypertrophy parameter,level of Ang II,express of bFGF and MAPK in heart were measured at 8week.Results:In experiment group,the blood pressure,cardiac hypertrophy parameter,Ang II,express of bFGF and MAPK significantly increased versus sham group at 8 week.The blood pressure,cardiac hypertrophy parameter,express of bFGF and MAPK distinctly decreased by losartan.Conclusion:The bFGF、MAPK may play a part role in the development of cardiac hypertrophy in renal hypertension.Losartan can inhibites the hypertrophic signal transduction induced by Ang II and bFGF