Differential Participation of Angiotensin II Type 1 and 2 Receptors in the Regulation of Cardiac Cell Death Triggered by Angiotensin II

被引：15

作者：

Aranguiz-Urroz, Pablo ^{[1
]}

Soto, Dagoberto ^{[1
]}

Contreras, Ariel ^{[1
]}

Troncoso, Rodrigo ^{[1
]}

Chiong, Mario ^{[1
]}

Montenegro, Jose ^{[1
]}

Venegas, Daniel ^{[1
]}

Smolic, Christian ^{[1
]}

Ayala, Pedro ^{[1
]}

Thomas, Walter G. ^{[2
]}

Lavandero, Sergio ^{[1
,3
]}

Diaz-Araya, Guillermo

机构：

[1] Univ Chile, Ctr FONDAP Estudios Mol Celula, Fac Ciencias Quim & Farmaceut, Santiago, Chile

[2] Univ Queensland, Sch Biomed Sci, Brisbane, Qld, Australia

[3] Univ Chile, Fac Med, Inst Ciencias Biomed, Santiago 7, Chile

来源：

AMERICAN JOURNAL OF HYPERTENSION | 2009年 / 22卷 / 05期

关键词：

VENTRICULAR MYOCYTES; AT(1) RECEPTOR; INDUCED HYPERTROPHY; AT(2) RECEPTOR; MUSCLE-CELL; HUMAN HEART; KINASE-C; IN-VITRO; ANG-II; FIBROBLASTS;

D O I：

10.1038/ajh.2009.32

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

BACKGROUND The Angiotensin II (Ang II) type 1 (AT(1)R) and type 2 (AT(2)R) receptors are increased in the heart following myocardial infarction and dilated cardiomyopathy, yet their contribution at a cellular level to compensation and/or failure remains controversial. METHODS We ectopically expressed AT(1)R and AT(2)R in cultured adult rat cardiomyocytes and cardiac fibroblasts to investigate Ang II-mediated cardiomyocyte hypertrophy and cardiac cell viability. RESULTS In adult rat cardiomyocytes, Ang II did not induce hypertrophy via the AT(1)R, and no effect of Ang II on cell viability was observed following AT(1)R or AT(2)R expression. In adult rat cardiac fibroblasts, Ang II stimulated cell death by apoptosis via the AT(1)R (but not the AT(2)R), which required the presence of extracellular calcium, and induced a rapid dissipation of mitochondrial membrane potential, which was significant from 8 h. CONCLUSIONS We conclude that Ang II/AT(1)R triggers apoptosis in adult rat cardiac fibroblasts, which is dependent on Ca2+ influx.

引用

页码：569 / 576

页数：8

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