高血压脑卒中患者血浆抗血管紧张素Ⅱ受体1型自身抗体的作用

Role of autoantibodies against angiotensinⅡtypy 1 receptor in hypertensive patients with cerebral stroke

目的:分析抗血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)受体1型(AT1)自身抗体与AngⅡ在高血压脑卒中的作用及其关系。方法:以合成的AT1-受体胞外第二环多肽片段作为抗原,用酶联免疫吸附试验法检测高血压脑卒中患者及正常人(各281例)血浆中的抗AT1-受体自身抗体,AngⅡ及肾素活性用放射免疫方法测定。结果:高血压脑卒中组抗AT1-受体自身抗体的阳性率(45.6%)显著高于对照组(9.3%,χ2=93.6,P<0.01);高血压脑卒中组及对照组血浆AngⅡ分别为(62.00±58.58)pmol/L和(42.70±28.65)pmol/L(t=4.962,P<0.01),肾素活性分别为(0.64±0.61)ng/(mL·h)和(0.46±0.44)ng/(mL·h)(t=4.027,P<0.01),均有显著差异。按脑卒中类型及脑卒中发病时间分组,抗AT1-受体自身抗体的阳性率、AngⅡ及肾素活性差异无显著意义;AngⅡ水平较高者抗AT1-受体自身抗体的阳性率显著高于AngⅡ较低者。结论:抗AT1-受体自身抗体、AngⅡ及肾素可能参与高血压脑卒中的进展,AngⅡ水平升高引起血管损伤可能是抗AT1-受体自身抗体产生的原因。

AIM:To analyze the effect of autoantibodies against angiotensinⅡ(AngⅡ) type 1(AT1) receptors and angiotensinⅡin hypertensive patients with cerebral stroke and analyze their relationship. METHODS:The peptides from the second extracellular loop of AT1-receptors were synthesized and used as antigens.The autoantibodies of the sera, which came from 281 hypertensive patients with cerebral stroke and 281 normotensives, were detected by using ELISA.The sera renin activity and AngII concentration were examined by radioimmunoassay. RESULTS:The positive rates of the autoantibodies against AT1-receptors, AngⅡconcentration and renin activity in the hypertensive group were 45.6%,(62.00±58.58) pmol/L and(0.64 ±0.61) ng/mL per hour,respectively,and all significantly higher than those in the normotensives group[9.3%,χ2=93.6,P< 0.01;(42.70±28.65) pmol/L,t=4.962, P< 0.01;(0.46 ±0.44) ng/mL per hour, t=4.027, P< 0.01].Among the subgroups of the stroke types and the episode time of stroke,the rates of the autoantibodies against AT1-receptors,Ang Ⅱconcentration and renin activity had no significant difference.In the stroke group,the positive rates of autoantibodies against AT1-receptors in the higher AngⅡlevel group was significantly higher than that in the lower AngⅡlevel. CONCLUSION:The autoantibodies against AT1-receptors,AngⅡand renin may play a role in the hypertensive patients with cerebral stroke, and the vascular damage caused by the increase of AngⅡmay be the reason of the occurrence of autoantibodies against AT1-receptors.