自发性高血压大鼠心肌胰岛素样生长因子-1受体基因表达与心血管细胞增殖

Myocardial insulin like growth factor-1 receptor gene expression and cardiovascular cell proliferation in SHR

目的 :观察自发性高血压大鼠(SHR)心肌胰岛素样生长因子 -1(IGF -1)受体基因表达水平 ,探讨其与心血管细胞增殖的病理机制以及福辛普利和氯沙坦治疗的影响。方法:24只SHR随机分3组 ,分别予福辛普利、氯沙坦和安慰剂灌胃治疗9周。检测尾动脉血压 ,测量心肌IGF -1受体mRNA水平并观察心肌、主动脉组织学改变。结果 :福辛普利组与氯沙坦组血压均显著低于对照组 ;其IGF -1受体mRNA水平均显著低于对照组 ,且血压与IGF -1受体mRNA水平呈正相关 ;光、电镜显示两治疗组较对照组心血管细胞增殖明显减轻 ,氯沙坦组增殖减轻更明显。结论:心肌IGF -1受体基因表达水平异常升高是导致SHR心血管细胞增殖的原因之一 ;福辛普利与氯沙坦均可有效控制血压 ,可能通过下调SHR心肌IGF -1受体的基因表达水平 。

Objective: To investigate the myocardial insulin-like growth factor-1(IGF-1) receptor gene expression in myocardium of Spontaneously Hypertensive Rat(SHR) as well as the pathology mechanism of the cardiovascular cell proliferation in the rats treated with Fosinpril and Losartan.Methods:24 SHR were divided randomly into 3 groups treated with Fosinpril, Losartan and placebo respectively by gastric perfusion for 9 weeks. Systolic blood pressure and mRNA levels of IGF-1 receptor of the three groups were measured.The changes of myocadium and abdominoartery in Histology were observed.Results:Compare to the control group,the BP level in Fosinpril group and Losartan group was significantly decreased, the mRNA levels of IGF-1 receptor were significantly decreased, the proliferation of the cardiovascular cell were significantly decreased and Losartan group was more than Fosinpril group. Blood pressure was significartly correlated to the mRNA levels of IGF-1 receptor. Conclusion: Abnormal increasement of the IGF-1 receptor gene expression in myocardium and abdomino_artery was one of the reasons result in SHR cardiovascular cell proliferation.Both Fosinpril and Losartan can control the BP effectively, decline the gene expression of IGF-1 receptor in myocardium and abdominoartery of SHR and through that, may restraine cardiovascular proliferation of the cardiovascular cell were significantly decreased and Losartan group was more than Fosinpril group.Blood pressure was significartly correlated to the mRNA levels of IGF-1 receptor.