In vivo key role of reactive oxygen species and NHE-1 activation in determining excessive cardiac hypertrophy

Growing in vitro evidence suggests NHE-1, a known target for reactive oxygen species (ROS), as a key mediator in cardiac hypertrophy (CH). Moreover, NHE-1 inhibition was shown effective in preventing CH and failure; so has been the case for AT1 receptor (AT1R) blockers. Previous experiments indicate...

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Autores principales:	Cingolani, Oscar H., Pérez, Néstor Gustavo, Ennis, Irene Lucía, Álvarez, María C., Mosca, Susana María, Schinella, Guillermo Raúl, Escudero, Eduardo Manuel, Console-Avegliano, Gloria Miriam, Cingolani, Horacio Eugenio
Formato:	Articulo
Lenguaje:	Inglés
Publicado:	2011
Materias:	Medicina Hypertrophy Sodium–hydrogen exchange Oxidative stress Angiotensin Phosphorylation
Acceso en línea:	http://sedici.unlp.edu.ar/handle/10915/132661
Aporte de:	SEDICI (UNLP) de Universidad Nacional de La Plata

id	I19-R120-10915-132661
record_format	dspace
institution	Universidad Nacional de La Plata
institution_str	I-19
repository_str	R-120
collection	SEDICI (UNLP)
language	Inglés
topic	Medicina Hypertrophy Sodium–hydrogen exchange Oxidative stress Angiotensin Phosphorylation
spellingShingle	Medicina Hypertrophy Sodium–hydrogen exchange Oxidative stress Angiotensin Phosphorylation Cingolani, Oscar H. Pérez, Néstor Gustavo Ennis, Irene Lucía Álvarez, María C. Mosca, Susana María Schinella, Guillermo Raúl Escudero, Eduardo Manuel Console-Avegliano, Gloria Miriam Cingolani, Horacio Eugenio In vivo key role of reactive oxygen species and NHE-1 activation in determining excessive cardiac hypertrophy
topic_facet	Medicina Hypertrophy Sodium–hydrogen exchange Oxidative stress Angiotensin Phosphorylation
description	Growing in vitro evidence suggests NHE-1, a known target for reactive oxygen species (ROS), as a key mediator in cardiac hypertrophy (CH). Moreover, NHE-1 inhibition was shown effective in preventing CH and failure; so has been the case for AT1 receptor (AT1R) blockers. Previous experiments indicate that myocardial stretch promotes angiotensin II release and post-translational NHE-1 activation; however, in vivo data supporting this mechanism and its long-term consequences are scanty. In this work, we thought of providing in vivo evidence linking AT1R with ROS and NHE-1 activation in mediating CH. CH was induced in mice by TAC. A group of animals was treated with the AT1R blocker losartan. Cardiac contractility was assessed by echocardiography and pressure–volume loop hemodynamics. After 7 weeks, TAC increased left ventricular (LV) mass by ~45% vs. sham and deteriorated LV systolic function. CH was accompanied by activation of the redox-sensitive kinase p90<sup>RSK</sup> with the consequent increase in NHE-1 phosphorylation. Losartan prevented p90<sup>RSK</sup> and NHE-1 phosphorylation, ameliorated CH and restored cardiac function despite decreased LV wall thickness and similar LV systolic pressures and diastolic dimensions (increased LV wall stress). In conclusion, AT1R blockade prevented excessive oxidative stress, p90<sup>RSK</sup> and NHE-1 phosphorylation, and decreased CH independently of hemodynamic changes. In addition, cardiac performance improved despite a higher work load.
format	Articulo Articulo
author	Cingolani, Oscar H. Pérez, Néstor Gustavo Ennis, Irene Lucía Álvarez, María C. Mosca, Susana María Schinella, Guillermo Raúl Escudero, Eduardo Manuel Console-Avegliano, Gloria Miriam Cingolani, Horacio Eugenio
author_facet	Cingolani, Oscar H. Pérez, Néstor Gustavo Ennis, Irene Lucía Álvarez, María C. Mosca, Susana María Schinella, Guillermo Raúl Escudero, Eduardo Manuel Console-Avegliano, Gloria Miriam Cingolani, Horacio Eugenio
author_sort	Cingolani, Oscar H.
title	In vivo key role of reactive oxygen species and NHE-1 activation in determining excessive cardiac hypertrophy
title_short	In vivo key role of reactive oxygen species and NHE-1 activation in determining excessive cardiac hypertrophy
title_full	In vivo key role of reactive oxygen species and NHE-1 activation in determining excessive cardiac hypertrophy
title_fullStr	In vivo key role of reactive oxygen species and NHE-1 activation in determining excessive cardiac hypertrophy
title_full_unstemmed	In vivo key role of reactive oxygen species and NHE-1 activation in determining excessive cardiac hypertrophy
title_sort	in vivo key role of reactive oxygen species and nhe-1 activation in determining excessive cardiac hypertrophy
publishDate	2011
url	http://sedici.unlp.edu.ar/handle/10915/132661
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In vivo key role of reactive oxygen species and NHE-1 activation in determining excessive cardiac hypertrophy

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