Sodium-hydrogen exchanger, cardiac overload, and myocardial hypertrophy

Autores
Cingolani, Horacio Eugenio; Ennis, Irene Lucía
Año de publicación
2007
Idioma
inglés
Tipo de recurso
reseña artículo
Estado
versión publicada
Descripción
Overload of neonatal and adult cardiomyocytes and multicellular myocardial preparations, which include whole hearts, are accompanied by an enhanced activity of the Na+/H+ exchanger 1 (NHE-1). Exogenous administration of prohypertrophic agents such as angiotensin II (Ang II), endothelin-1 (ET-1), and α1-adrenergic agonists also stimulates NHE-1 activity, which leads to an increased concentration of intracellular Na+ ([Na+]i). Moreover, inhibition of NHE-1 activity prevents the increase in [Na+]i, induces the regression of cardiac hypertrophy, and exerts beneficial effects in experimental heart failure. The present review summarizes the current knowledge of the causative factors and pathophysiological correlation of cardiac overload and NHE-1 activity.
Centro de Investigaciones Cardiovasculares
Materia
Ciencias Médicas
Hypertrophy
Signal transduction
Sodium
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/83235
Acceder
id SEDICI_9147ffaf75ec2a9526da7e2bc3768ed8
oai_identifier_str oai:sedici.unlp.edu.ar:10915/83235
network_acronym_str SEDICI
repository_id_str 1329
network_name_str SEDICI (UNLP)
spelling Sodium-hydrogen exchanger, cardiac overload, and myocardial hypertrophyCingolani, Horacio EugenioEnnis, Irene LucíaCiencias MédicasHypertrophySignal transductionSodiumOverload of neonatal and adult cardiomyocytes and multicellular myocardial preparations, which include whole hearts, are accompanied by an enhanced activity of the Na+/H+ exchanger 1 (NHE-1). Exogenous administration of prohypertrophic agents such as angiotensin II (Ang II), endothelin-1 (ET-1), and α1-adrenergic agonists also stimulates NHE-1 activity, which leads to an increased concentration of intracellular Na+ ([Na+]i). Moreover, inhibition of NHE-1 activity prevents the increase in [Na+]i, induces the regression of cardiac hypertrophy, and exerts beneficial effects in experimental heart failure. The present review summarizes the current knowledge of the causative factors and pathophysiological correlation of cardiac overload and NHE-1 activity.Centro de Investigaciones Cardiovasculares2007info:eu-repo/semantics/reviewinfo:eu-repo/semantics/publishedVersionRevisionhttp://purl.org/coar/resource_type/c_dcae04bcinfo:ar-repo/semantics/resenaArticuloapplication/pdfhttp://sedici.unlp.edu.ar/handle/10915/83235enginfo:eu-repo/semantics/altIdentifier/issn/0009-7322info:eu-repo/semantics/altIdentifier/doi/10.1161/CIRCULATIONAHA.106.626929info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-03T10:48:00Zoai:sedici.unlp.edu.ar:10915/83235Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-03 10:48:01.037SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Sodium-hydrogen exchanger, cardiac overload, and myocardial hypertrophy
title Sodium-hydrogen exchanger, cardiac overload, and myocardial hypertrophy
spellingShingle Sodium-hydrogen exchanger, cardiac overload, and myocardial hypertrophy
Cingolani, Horacio Eugenio
Ciencias Médicas
Hypertrophy
Signal transduction
Sodium
title_short Sodium-hydrogen exchanger, cardiac overload, and myocardial hypertrophy
title_full Sodium-hydrogen exchanger, cardiac overload, and myocardial hypertrophy
title_fullStr Sodium-hydrogen exchanger, cardiac overload, and myocardial hypertrophy
title_full_unstemmed Sodium-hydrogen exchanger, cardiac overload, and myocardial hypertrophy
title_sort Sodium-hydrogen exchanger, cardiac overload, and myocardial hypertrophy
dc.creator.none.fl_str_mv Cingolani, Horacio Eugenio
Ennis, Irene Lucía
author Cingolani, Horacio Eugenio
author_facet Cingolani, Horacio Eugenio
Ennis, Irene Lucía
author_role author
author2 Ennis, Irene Lucía
author2_role author
dc.subject.none.fl_str_mv Ciencias Médicas
Hypertrophy
Signal transduction
Sodium
topic Ciencias Médicas
Hypertrophy
Signal transduction
Sodium
dc.description.none.fl_txt_mv Overload of neonatal and adult cardiomyocytes and multicellular myocardial preparations, which include whole hearts, are accompanied by an enhanced activity of the Na+/H+ exchanger 1 (NHE-1). Exogenous administration of prohypertrophic agents such as angiotensin II (Ang II), endothelin-1 (ET-1), and α1-adrenergic agonists also stimulates NHE-1 activity, which leads to an increased concentration of intracellular Na+ ([Na+]i). Moreover, inhibition of NHE-1 activity prevents the increase in [Na+]i, induces the regression of cardiac hypertrophy, and exerts beneficial effects in experimental heart failure. The present review summarizes the current knowledge of the causative factors and pathophysiological correlation of cardiac overload and NHE-1 activity.
Centro de Investigaciones Cardiovasculares
description Overload of neonatal and adult cardiomyocytes and multicellular myocardial preparations, which include whole hearts, are accompanied by an enhanced activity of the Na+/H+ exchanger 1 (NHE-1). Exogenous administration of prohypertrophic agents such as angiotensin II (Ang II), endothelin-1 (ET-1), and α1-adrenergic agonists also stimulates NHE-1 activity, which leads to an increased concentration of intracellular Na+ ([Na+]i). Moreover, inhibition of NHE-1 activity prevents the increase in [Na+]i, induces the regression of cardiac hypertrophy, and exerts beneficial effects in experimental heart failure. The present review summarizes the current knowledge of the causative factors and pathophysiological correlation of cardiac overload and NHE-1 activity.
publishDate 2007
dc.date.none.fl_str_mv 2007
dc.type.none.fl_str_mv info:eu-repo/semantics/review
info:eu-repo/semantics/publishedVersion
Revision
http://purl.org/coar/resource_type/c_dcae04bc
info:ar-repo/semantics/resenaArticulo
format review
status_str publishedVersion
dc.identifier.none.fl_str_mv http://sedici.unlp.edu.ar/handle/10915/83235
url http://sedici.unlp.edu.ar/handle/10915/83235
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/issn/0009-7322
info:eu-repo/semantics/altIdentifier/doi/10.1161/CIRCULATIONAHA.106.626929
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:SEDICI (UNLP)
instname:Universidad Nacional de La Plata
instacron:UNLP
reponame_str SEDICI (UNLP)
collection SEDICI (UNLP)
instname_str Universidad Nacional de La Plata
instacron_str UNLP
institution UNLP
repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
repository.mail.fl_str_mv alira@sedici.unlp.edu.ar
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score 13.13397

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