Objective    To study the effect of electroporation-mediated in vivo local transfection of angiotensin Ⅱ type 2 receptor (AT2R) gene on neointi

mal hyperplasia in rat common carotid arteries after balloon angioplasty.     Methods     Seventy-two healthy SD rats were randomly and evenly divided into a control group

an injured group

an empty plasmid group (pEGFP-N

2

group)

and an AT2R transfection group (pEGFP-AT2R group). Balloon catheter denudation of the endothelia of rat common carotid arteries was routinely used to construct a restenosis model. The transfection of plasmids pEGFP-AT2R and pEGFP-N

2

was carried out by local electroporation. The injured arteries were collected 7 d

14 d

and 21 d after transfection. AT2R and angiotensin Ⅱ type 1 receptor (AT1R) expression levels in the carotid artery walls as well as histomorphological characteristics were analyzed with RT-PCR and HE staining. The effect of AT2R on neointimal hyperplasia of in vivo arteries was evaluated.     Results    The AT2R mRNA expression level in the injured rat common carotid arteries of the pEGFP-AT2R group was (1.262±0.317)

indicating remarkable difference from those of the pEGFP-N

2

group (0.396±0.100) and injured group (0.410±0.053) 21 d after transfection (P0.01). The AT1R mRNA expression level in the pEGFP-AT2R group was 0.469±0.065

statistically higher than those of the pEGFP-N

2

group (0.363±0.046) and injured group (0.373±0.045) 21 d after transfection (P0.05). The intima-to-media (I/M) area ratio of the pEGFP-AT2R group (0.828±0.101) showed obvious difference from those of the pEGFP-N

2

group (1.432±0.086) and injured group (1.515±0.078) 21 d after transfection (P0.01). Compared with the injured group

AT2R transfection in the pEGFP-AT2R group inhibited neointimal hyperplasia in experimental animals at a rate as high as 45.35%.     Conclusion    Electroporation-mediated in vivo AT2R gene transfection can significantly up-regulate AT2R expression in injured common carotid artery tissues of rats. There is no negative correlation between the expression levels of AT2R and AT1R.