血管紧张素Ⅱ受体在压力超负荷致左室肥大中的作用

目的:探讨血管紧张素Ⅱ受体(ATRs)在压力超负荷致左室肥大中的作用。 方法:采用大鼠腹主动脉缩窄模型,通过放免法测心肌组织血管紧张素Ⅱ(Ang Ⅱ)含量,放射性配基结合分析法检测心肌组织ATRs及其亚型的变化。结果:手术组AngⅡ含量显著增高,与左室重量指数(LVMI)呈正相关(r=0.8066,P<0.01)。ATRs最大结合容量 (Bmax) 显著高于对照组(P＜0.01),但两组之间的平衡解离常数(kd)、血管紧张素Ⅱ1型受体(AT₁R)和血管紧张素Ⅱ2型受体(AT₂R)之间的比例无显著差异。非肽类AT₁R 拮抗剂Irbesartan可显著抑制Ang Ⅱ的升高和左室肥大,非肽类AT₂R 拮抗剂CGP42112A则无此作用。结论: 压力超负荷时心肌组织ATRs上调,Ang Ⅱ致左室肥大的作用主要由AT₁R介导。

Role of angiotensin

AIM and METHODS： To investigate the role of angiotensin Ⅱrecepters(ATRs) in overload pressure-induced left ventricular hypertrophy. The rat abdominal aortic constraction model was adopted. At 10th week after operating, angiotensin Ⅱ in myocardium was measured by radioimmunoassay,tissue ATRs and its subtype were analysed by radioligand binding assay. RESULTS: The AngⅡ content in the operated group was significantly higher than that of the control group, LVMI was positively correlated with AngⅡ(r=0.8066,P＜0.01).The maximal binding capacity of ATRs in the operated group was significantly higher than that of the control group(P＜0.01). However,the equilibrium dissociation constant(kd) and ratio of AT1R to AT2R in these two groups had no significantly different. Left ventricular hypertrophy was significantly reduced by AT1R antagonist irbesartan,and not influenced by AT2R antagonist CGP42112A. CONCLUSION: These results suggested that left ventricular ATRs upregulate during pressure overload.The left ventricular hypertrophy induced by AngⅡis mainly mediated by AT1R.