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血管紧张素Ⅱ诱导培养的成年大鼠心肌细胞凋亡

郭迅, 郭兆贵

湖南医科大学分子药理研究室

摘要

研究血管紧张素Ⅱ（AugⅡ）诱导培养的成年大鼠心肌细胞（adultratventricularmyocytos，ARVMs）凋亡。酶灌流消化法分离培养ARVMs，不同处理后，光镜观察形态改变，琼脂糖凝胶电泳定性分析DNA降解程度。结果发现培养的ARVMs经AugⅡ10μmol／L处理48h后，大部分细胞变圆，胞浆浓缩；电泳显示核酸断裂片段“梯形”结构，上述改变在72h更为明显。上述作用可被氯沙坦、维拉帕米和staureporine所取消。这表明AngⅡ由AT1受体介导诱导培养的ARVMs凋亡，细胞内钙升高和PKC激活起重要作用。

关键词： 血管紧张素Ⅱ; 凋亡; 氯沙坦; 心肌细胞; 大鼠

Cui Hong

First Clinical Institute，China Medical University. Shenyang 110001,Liaoning, China

Abstract

Angiotensin　Ⅱ(AngⅡ)-induced apoptosis was demonstrated for the first time in cultured adult rat ventricular myocytes (ARWs) isolated by retrograde heart perfusion with Krebs-Henseleit bicarbonate (KHB) buffer containing collagenase and hyaluronidase. ARWs incubated with 10μmol/L Ang Ⅱ for 48 h showed morphological features of apoptosis (cellular shrinkage, condensation of cytoplasm) and a characteristic "ladder" of DNA bands representing integer multiples of the intermucleosomal DNA length about 180~200 hp; which became more evident with further incubation up to 72 h. With shorter incubation time (≤24 h) or at a lower AngⅡconcentration (<10μmol/L), such changes failed to occur. This effect of Ang Ⅱ could be abolished by losartan (10μmol/L), verapamil (1μmol/L) or staurosporine (10 nmol/L). The above results indicate that AngⅡ-induced apoptosis in ARVMs may be mainly mediated by AngⅡ type Ⅰ(AT1) receptors with [Cd+ ]i and protein kinase C (PKC) playing a critical role.

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引用本文：

郭迅, 郭兆贵. 血管紧张素Ⅱ诱导培养的成年大鼠心肌细胞凋亡[J]. 生理学报 1998; 50 (4): .

Cui Hong. . Acta Physiol Sin 1998; 50 (4): (in Chinese with English abstract).