血管紧张素Ⅱ对心肌缝隙连接蛋白43重构的影响及贝那普利的干预作用

Effect of angiotensinⅡand benazepril on remodeling of cardiac gap junction connexin43

目的采用大鼠肾上腹主动脉部分结扎的模型,观察心肌缝隙连接蛋白(Connexin,Cx)43含量和分布的变化以及贝那普利干预的防治效果。方法将30只雄性Wistar大鼠随机等分为对照组(A组)、腹主动脉结扎组(B组)、结扎+贝那普利组(C组)。喂养8周后处死,用放射免疫法测定血浆血管紧张素Ⅱ(AngⅡ)浓度和心肌组织AngⅡ浓度,用免疫组化方法显示大鼠心肌Cx43的分布特征,半定量统计分析。结果与A组相比,B组大鼠血浆、心肌AngⅡ浓度显著升高(均P<0.01),但B组大鼠心房肌及心室肌Cx43含量均较A组显著减少(分别为P<0.05和P<0.01),且分布紊乱;而C组Cx43含量较B组显著增多(P<0.01),且分布不规律程度减轻。结论AngⅡ升高可能导致心肌Cx43重新分布及表达减少;贝那普利能有效减轻Cx43的重构。

AIM To investigate the effect of angiotensin Ⅱ （Ang Ⅱ ）and benazepril on the level and distribution changes of connexin43 （Cx43） in rats with suprarenal abdominal aorta banded, METHODS Thirty male Wistar rats were randomly divided into control group（ A）, abdominal aorta banded group（B） and abdominal aorta banded plus benazepril group （C）. The plasma and myocardium concentration of Ang Ⅱ was determined by radioimmunoassay after eight weeks. Cx43 was detected with immunohistochemical method and was semi-quantitatively analyzed in different groups. RESULTS The plasma and myocardium concentration of Ang Ⅱ increased markedly （ P 〈 0.01 ） but the Cx43 protein level of atrial and ventricular tissue in group B decreased significantly （ P 〈 0.05 and P 〈 0.01 , respectively） with misdistribution compared with those in group A. Cx43 level increased significantly（ P 〈 0.01 ） in group C compared with that in group B and the inhomogeneity in Cx43 distribution decreased. CONCLUSION The results show that Cx43 remodeling with redistribution and reduction of protein expression may be induced by the increase of Ang Ⅱ level and benazepril attenuates Cx43 remodeling effectively.