TY - JOUR
T1 - Differential participation of angiotensin II type 1 and 2 receptors in the regulation of cardiac cell death triggered by angiotensin II
AU - Aránguiz-Urroz, Pablo
AU - Soto, Dagoberto
AU - Contreras, Ariel
AU - Troncoso, Rodrigo
AU - Chiong, Mario
AU - Montenegro, José
AU - Venegas, Daniel
AU - Smolic, Christian
AU - Ayala, Pedro
AU - Thomas, Walter G.
AU - Lavandero, Sergio
AU - Díaz-Araya, Guillermo
N1 - Funding Information:
Supplementary material is linked to the online version of the paper at http:// www.nature.com/ajh acknowledgments: This research was supported by grants from Fondo Nacional de Desarrollo Científico y Tecnológico (FONDECyT) 1061059 (to G.D.a) and Fondo de areas Prioritarias (FONDaP) 15010006 (to S.L.). D.S., P.a., a.C., R.T., and M.C. hold a PhD fellowship from Consejo Nacional de Ciencia y Tecnologia (CONICyT), Chile.
PY - 2009/5/1
Y1 - 2009/5/1
N2 - Background: The Angiotensin II (Ang II) type 1 (AT"1R) and type 2 (AT"2R) 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.MethodsWe ectopically expressed AT"1R and AT"2R in cultured adult rat cardiomyocytes and cardiac fibroblasts to investigate Ang II-mediated cardiomyocyte hypertrophy and cardiac cell viability.ResultsIn adult rat cardiomyocytes, Ang II did not induce hypertrophy via the AT"1R, and no effect of Ang II on cell viability was observed following AT"1R or AT"2R expression. In adult rat cardiac fibroblasts, Ang II stimulated cell death by apoptosis via the AT"1R (but not the AT"2R), which required the presence of extracellular calcium, and induced a rapid dissipation of mitochondrial membrane potential, which was significant from 8 h.ConclusionsWe conclude that Ang II/AT"1R triggers apoptosis in adult rat cardiac fibroblasts, which is dependent on Ca2+ influx.
AB - Background: The Angiotensin II (Ang II) type 1 (AT"1R) and type 2 (AT"2R) 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.MethodsWe ectopically expressed AT"1R and AT"2R in cultured adult rat cardiomyocytes and cardiac fibroblasts to investigate Ang II-mediated cardiomyocyte hypertrophy and cardiac cell viability.ResultsIn adult rat cardiomyocytes, Ang II did not induce hypertrophy via the AT"1R, and no effect of Ang II on cell viability was observed following AT"1R or AT"2R expression. In adult rat cardiac fibroblasts, Ang II stimulated cell death by apoptosis via the AT"1R (but not the AT"2R), which required the presence of extracellular calcium, and induced a rapid dissipation of mitochondrial membrane potential, which was significant from 8 h.ConclusionsWe conclude that Ang II/AT"1R triggers apoptosis in adult rat cardiac fibroblasts, which is dependent on Ca2+ influx.
UR - http://www.scopus.com/inward/record.url?scp=67349089992&partnerID=8YFLogxK
U2 - 10.1038/ajh.2009.32
DO - 10.1038/ajh.2009.32
M3 - Article
C2 - 19300422
AN - SCOPUS:67349089992
SN - 0895-7061
VL - 22
SP - 569
EP - 576
JO - American Journal of Hypertension
JF - American Journal of Hypertension
IS - 5
ER -