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

2009; Oxford University Press; Volume: 22; Issue: 5 Linguagem: Inglês

10.1038/ajh.2009.32

1941-7225

Pablo Aránguiz, Dagoberto Soto, Ariel Contreras‐Ferrat, Rodrigo Troncoso, Mario Chiong, José Luis Cadena Montenegro, Daniel Venegas, Christian Smolic, Pedro Ayala, Walter G. Thomas, Sergio Lavandero, Guillermo Díaz‐Araya,

Ion channel regulation and function

The Angiotensin II (Ang II) type 1 (AT1R) and type 2 (AT2R) 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. We ectopically expressed AT1R and AT2R in cultured adult rat cardiomyocytes and cardiac fibroblasts to investigate Ang II-mediated cardiomyocyte hypertrophy and cardiac cell viability. In adult rat cardiomyocytes, Ang II did not induce hypertrophy via the AT1R, and no effect of Ang II on cell viability was observed following AT1R or AT2R expression. In adult rat cardiac fibroblasts, Ang II stimulated cell death by apoptosis via the AT1R (but not the AT2R), which required the presence of extracellular calcium, and induced a rapid dissipation of mitochondrial membrane potential, which was significant from 8 h. We conclude that Ang II/AT1R triggers apoptosis in adult rat cardiac fibroblasts, which is dependent on Ca2+ influx.