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Chinese Archives of General Surgery(Electronic Edition) ›› 2009, Vol. 03 ›› Issue (04): 285-288. doi: 10.3877/cma.j.issn.1674-0793.2009.04.006

• Original Articles • Previous Articles     Next Articles

Expression of AngII receptors in rat injured aorta and it's significance in neointimal hyperplasia

Jian-wen LI1, Shui-chuan HUANG1, San-ming WANG1, Yuan-qi ZHANG1, Xiao-dong CHEN1,()   

  1. 1.Deptartment of Vascular Surgery, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, China
  • Received:2008-06-24 Online:2009-08-01 Published:2024-11-29
  • Contact: Xiao-dong CHEN

Abstract:

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.

Key words: AT1R, AT2R, Neointimal hyperplasia, Injured

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