肾血管性高血压大鼠发病过程中心血管AT_1-受体自身抗体的变化  

Changes in autoantibody against cardiovascular AT_1-receptor during development of renovascular hypertension in rats

作　　者：支建明[1] 赵录英[1] 焦向英[1] 赵荣瑞[1] 

机构地区：[1]山西医科大学心血管生理研究室,太原030001

出　　处：《生理学报》2002年第4期317-320,共4页Acta Physiologica Sinica

摘　　要：实验观察了肾血管性高血压（RVH）大鼠血浆中抗AT1-受体自身抗体在发病过程中的作用及其变化规律。采用两肾一夹Goldblatt RVH模型,以合成的大鼠AT1-受体细胞外第二环165-191位氨基酸序列作为特异性抗原,用SA-ELISA法检测大鼠血清中抗AT1-受体自身抗体。结果表明,RVH模型组术后2周时大鼠血清中抗AT1-受体自身抗体的阳性率和平均滴度与术前相比明显增高,较高的阳性率和平均滴度持续几周后逐渐下降,12周时下降到正常水平。结果提示,自身免疫机制参与了高血压的形成,抗AT1-受体自身抗体可能与心肌肥厚有关。The aim of this study was to observe the change in angiotensin Ⅱ receptor subtype 1 ( AT1) autoantibody during the development of renovascular hypertension ( RVH) . The Goldblatt renovascular hypertension model was established by the two-kidney one-clip method, and a synthetic peptide corresponding to amino acid sequence 165-191 of the second extracellular loop of the AT1-receptor was used as the antigen. Sera AT1-receptor autoantibody was detected by SA-ELISA. It was shown that two weeks after operation both the frequency of occurrence and the titre of autoantibodies to AT1 -receptor were significantly increased as compared with the pre-treatment control. The increase in autoantibodies lasted several weeks and then decreased gradually to the pre-clipping level at 12 weeks. It is suggested that autoimmune mechanisms are involved in the pathogenesis of renovascular hypertension and the AT1 autoantibodies may be one of the mechanisms leading to cardiac hypertrophy.

关 键 词：肾血管性高血压 大鼠 发病过程 心血管AT1-受体 血管紧张素Ⅱ 自身抗体 

分 类 号：R544.1[医药卫生—心血管疾病]