血管球囊损伤后血管紧张素Ⅱ受体在内膜增生中的作用  

Role of angiotensin II receptor in neointima hyperplasia after vascular balloon injury

作　　者：程训民[1] 何国祥[1] 王国超[1] 

机构地区：[1]第三军医大学附属西南医院心内科

出　　处：《中华心血管病杂志》1998年第2期142-144,共3页Chinese Journal of Cardiology

摘　　要：目的探讨血管紧张素Ⅱ受体（ＡＴＲ）在血管球囊损伤后内膜增生中的作用。方法用放射配基结合分析法测定损伤后血管组织ＡＴＲ及其亚型的变化；免疫组化方法测定增殖细胞核抗原（ＰＣＮＡ）阳性细胞以了解血管内膜增殖过程。结果内膜损伤后第３天组织中ＡＴＲ显著增高（Ｐ＜０．０５）；第１４天ＡＴＲ的最大结合容量是对照组的３倍，而受体的平衡解离常数无显著变化；第２８天组织ＡＴＲ降至基础水平。增高的ＡＴＲ为血管紧张素Ⅱ１型受体（ＡＴ１Ｒ）。非肽类ＡＴ１Ｒ拮抗剂Ｉｒｂｅｓａｒｔａｎ显著抑制血管平滑肌细胞增殖，减少新生内膜面积；非肽类血管紧张素Ⅱ２型受体（ＡＴ２Ｒ）拮抗剂ＣＧＰ４２１１２Ａ则无此作用。结论血管内皮损伤后ＡＴＲ上调，ＡＴ１Ｒ参与血管内皮损伤后内膜增殖。Objective To investigate the role of angiotensin Ⅱ receptor(ATR) in neointima hyperplasia after vascular balloon injury in rat models. Methods Tissue ATR and ATR subtype was measured by the radioligand binding assay. Proliferation cellular nuclear antigen (PCNA) was observed by means of immunohistochemistry technique after vascular balloon injury to study the proliferation of vascular smooth muscle cells (VSMC).Results ATR increased significantly at day 3 ( P <0.05), the maximal binding capacity of receptor in injury artery ( n =8) was 3 times as those in the control group ( n =8) at day 14 and recovered at day 28 after vascular balloon injury. However, its equilibrium dissociation constant was not significantly changed ( P >0.05). ATR in the normal and proliferating iliac artery was exclusively angiotensin Ⅱ type 1 receptor (AT 1R). Irbesartan, a non peptide AT 1R antagonist, inhibited significantly the proliferation of VSMC and attenuated the neointima area. However, CGP42112A, a non peptide angiotensin Ⅱ type 2 receptor (AT 2R) antagonist, had no effect on neointima hyperplasia. Conclusion ATR upregulates, and AT 1R is involved in neointima hyperplasia after vascular balloon injury.

关 键 词：血管紧张素Ⅱ 受体 血管内膜 损伤 动脉硬化 

分 类 号：R543.502[医药卫生—心血管疾病]