摘要(Abstract)：

<正> Objective:To investigate the role of angiotensin Ⅱ receptor(ATR) inneointima hyperplasia after vascular balloon injury.Methods:The tissueATR and ATR subtype was measured by the radioligand binding essay.Inorder to understard the proliferous procesa of vascular smooth muscle cells(VSMC),the proliferation cellular nuclear antigen(PCNA) was observedby means of immunohistochemistry techniqu in the rats model aftervascular balloon injury.Results:The ATR increased significantly at day 3(P<0.05),the maximal binding capacity of receptor in injury artery was 3times as those in the control group at day 14 and recovered at day 28 aftervascular balloon injury.However,its equilibrium dissociation contantwas not significantly change(P>0.05).The ATR in normal andproliferating iliac artery was exclusively angiotensin Ⅱ type 1 receptor(ATIR).Irbesattan,a non-peptide ATIR antagonist,inhibited significantlythe proliferation of VSMC and attenuated neointima area However,CGP42112A,a non-peptide angiotensin Ⅱ type 2 receptor(AT2R)antagonist,had no effect on neointima hyperplasia.Conclusions:ATRupregulates,and ATIR is involved in neointima hyperplasia aftervascular balloon injury.

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