Differential participation of angiotensin II type 1 and 2 receptors in the regulation of cardiac cell death triggered by angiotensin II

Pablo Aránguiz-Urroz; Dagoberto Soto; Ariel Contreras; Rodrigo Troncoso; Mario Chiong; José Montenegro; Daniel Venegas; Christian Smolic; Pedro Ayala; Walter G. Thomas; Sergio Lavandero; Guillermo Díaz-Araya

doi:10.1038/ajh.2009.32

Differential participation of angiotensin II type 1 and 2 receptors in the regulation of cardiac cell death triggered by angiotensin II

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

Universidad de Chile

Producción científica › revisión exhaustiva

15 Citas (Scopus)

Resumen

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.

Idioma original	English
Páginas (desde-hasta)	569-576
Número de páginas	8
Publicación	American Journal of Hypertension
Volumen	22
N.º	5
DOI	https://doi.org/10.1038/ajh.2009.32
Estado	Published - may. 2009

Financiación

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.

Financiadores	Número del financiador
Consejo Nacional de Ciencia y Tecnologia
Fondo Nacional de Desarrollo Científico y Tecnológico	1061059, 15010006

ASJC Scopus Subject Areas

Internal Medicine

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Aránguiz-Urroz, P., Soto, D., Contreras, A., Troncoso, R., Chiong, M., Montenegro, J., Venegas, D., Smolic, C., Ayala, P., Thomas, W. G., Lavandero, S., & Díaz-Araya, G. (2009). Differential participation of angiotensin II type 1 and 2 receptors in the regulation of cardiac cell death triggered by angiotensin II. American Journal of Hypertension, 22(5), 569-576. https://doi.org/10.1038/ajh.2009.32

Aránguiz-Urroz, P, Soto, D, Contreras, A, Troncoso, R, Chiong, M, Montenegro, J, Venegas, D, Smolic, C, Ayala, P, Thomas, WG, Lavandero, S & Díaz-Araya, G 2009, 'Differential participation of angiotensin II type 1 and 2 receptors in the regulation of cardiac cell death triggered by angiotensin II', American Journal of Hypertension, vol. 22, n.º 5, pp. 569-576. https://doi.org/10.1038/ajh.2009.32

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title = "Differential participation of angiotensin II type 1 and 2 receptors in the regulation of cardiac cell death triggered by angiotensin II",

abstract = "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.",

author = "Pablo Ar{\'a}nguiz-Urroz and Dagoberto Soto and Ariel Contreras and Rodrigo Troncoso and Mario Chiong and Jos{\'e} Montenegro and Daniel Venegas and Christian Smolic and Pedro Ayala and Thomas, {Walter G.} and Sergio Lavandero and Guillermo D{\'i}az-Araya",

note = "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 Cient{\'i}fico y Tecnol{\'o}gico (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.",

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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

Y1 - 2009/5

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.

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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

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