缬沙坦对血管紧张素Ⅱ诱导的肥大心肌细胞胞内钙的影响  

Valsartan suppresses the increase of [Ca^(2+)]i in angiotensin Ⅱ induced hypertrophic cardiocytes

作　　者：程冕[1] 张存泰[1] 宋玉娥[1] 王琳[1] 吕家高[1] 王岚[1] 刘念[1] 阮燕菲[1] 白融[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院心内科

出　　处：《临床心血管病杂志》2008年第9期695-697,共3页Journal of Clinical Cardiology

基　　金：国家自然科学基金资助课题(No:30470714)

摘　　要：目的:观察血管紧张素Ⅱ(AngⅡ)1型受体(AT1)拮抗剂缬沙坦(Valsartan)对AngⅡ诱导的肥大心肌细胞胞内钙([Ca2+]i)变化的影响,并探讨其机制。方法:原代培养的大鼠心肌细胞,3H-亮氨酸掺入法测定心肌细胞蛋白质合成速率,利用共聚焦显微镜技术测定[Ca2+]i。结果:AngⅡ诱导心肌细胞肥大48h后[Ca2+]i明显增加,与空白对照组比较差异有统计学意义(P<0.01);缬沙坦预处理后,[Ca2+]i与肥大组相比下降,差异有统计学意义(P<0.01),与空白对照组相比,差异无统计学意义(P>0.05)。结论:AngⅡ诱导肥大心肌细胞[Ca2+]i增加,缬沙坦通过阻断AT1受体,抑制肥大心肌细胞[Ca2+]i增加。Objective：To explore the effects of valsartan on the level of [Ca^2＋ ]i in angiotensin Ⅱ induced hypertrophic cardiocytes. Method： Primary cultured neonatal rat cardiocytes were cultured. The protein synthesis rate in cultured eardiocytes was determined by the ^3 H-leucine incorporation. [Ca^2＋ ]i concentration was measured with laser confocal microscopy. Result： Hypertrophic cardiocytes were induced by angiotensin Ⅱ. After a 48 hour treatment, the level of [Ca^2＋ ]i was increased significantly compared with the control （P〈0.01） whereas it de creased significantly（P〈0.01） with preconditioning valsartan. There was no significant difference on the level of [Ca^2＋ ]i in valsartan and control groups（P〉0.05）. Conclusion：Angiotensin Ⅱ induces the increase [Ca^2＋ ]i in hypertrophic cardiocytes. Valsartan may suppress the level of [Ca^2＋ ]i through blocking the AT1 receptor.

关 键 词：缬沙坦 心肌细胞 肥大 细胞内游离钙 血管紧张素Ⅱ 

分 类 号：R972.4[医药卫生—药品]