目的

探讨血管成形术后新生内膜增生过程中血管紧张素II受体（AT1R、AT2R）间的相互关系。

方法

以SD大鼠胸主动脉球囊损伤模型，应用AT1R、AT2R和胞外信号调控激酶1（ERK1）受体阻断剂进行干预，分正常组、单纯损伤组、PD123319组、valsartan组、PD98059组、valsartan+PD98059组，于术后14 d取材，用RT-PCR和蛋白免疫印迹杂交法检测AT1R、AT2R、ERK1 mRNA和蛋白质在血管中的表达变化。

结果

单纯损伤组、PD123319组和PD98059组AT1R mRNA和蛋白表达明显强于正常组、valsartan组、valsartan+PD98059组（P<0.05），经PD123319阻断AT2R后，AT1R mRNA和蛋白表达量与单纯损伤组相比无明显差异。正常组血管壁中无AT2R mRNA和蛋白表达，经valsartan阻断AT1R后，AT2R mRNA和蛋白表达量与单纯损伤组相比无明显差异。

结论

在抑制新生内膜增生过程中，AT1R和AT2R两者间并不存在表达量上的此消彼长，可能是建立在信号转导基础上的功能调节关系，推测AT2R通过灭活AT1R激活的ERK1，从而抑制新生内膜增生。

Objective

To study the mutual function relations of AT1R and AT2R in post angioplasty neointimal hyperplasia.

Methods

After establishment of rat carotid balloon injury restenosis model,valsartan,D123319,D98059 were used into rat carotid arteries.The rats were divided into normal,injured,PD123319,valsartan,PD98059,valsartan+PD98059 groups.The arteries were harvested at 14 days.The expressions of AT2R,AT1R,extracellular regulated kinase(ERK1)were evaluated with RT-PCR and western blotting.

Results

The expressions of AT1R mRNA and protein in injured, PD123319 and PD98059 group were stronger than those in normal,valsartan and valsartan+PD98059 groups (P<0.05).There was not significant change of AT1R mRNA or protein after AT2R was blocked by PD123319 compare with group injured. There was not expression of AT2R mRNA or protein in the normal group blood vessel wall.No significant change of AT2R mRNA and protein after AT1R was blocked by valsartan compare with group injured.

Conclusions

In the suppressing course of neointimal hyperplasia,the relation of AT1R between AT2R is not likes"As one falls,another rises"，but maybe establishes on the foundation of signal transduction.We infer that AT2R inactivate ERK1 which is activated by AT1R,thus to suppress neointimal hyperplasia.