Increased Na+ /Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats

Autores
Rodriguez, Jesica S.; Velez Rueda, Jorge Omar; Salas, Margarita; Becerra, Romina Valeria; Di Carlo, Mariano Nahuel; Said, Maria Matilde; Vittone, Leticia Beatriz; Rinaldi, Gustavo Juan; Portiansky, Enrique Leo; Mundiña, Cecilia Beatriz; Palomeque, Julieta; Mattiazzi, Ramona Alicia
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Spontaneously hypertensive rat (SHR) constitutes a genetic model widely used to study the natural evolution of hypertensive heart disease. Ca2+ -handling alterations are known to occur in SHR. However, the putative modifications of Ca2+ -handling proteins during the progression to heart failure (HF) are not well established. Moreover, the role of apoptosis in SHR is controversial. We investigated intracellular Ca2+ , Ca2+ -handling proteins and apoptosis in SHR vs. control Wistar rats (W) from 3 to 15 months (mo). Changes associated with the transition to HF (i.e. lung edema and decrease in midwall fractional shortening), occurred at 15 mo in 38% of SHR (SHRF). In SHRF, twitch and caffeine-induced Ca2+ transients, significantly decreased relative to 6/9 mo and 15 mo without HF signs. This decrease occurred in association with a decrease in the time constant of caffeine-Ca2+ transient decay and an increase in Na+ /Ca2+ exchanger (NCX) abundance (p, 0.05) with no changes in SERCA2a expression/activity. An increased Ca2+ -calmodulin-kinase II activity, associated with an enhancement of apoptosis (TUNEL and Bax/Bcl2) was observed in SHR relative to W from 3 to 15 mo. Conclusions: 1. Apoptosis is an early and persistent event that may contribute to hypertrophic remodeling but would not participate in the contractile impairment of SHRF. 2. The increase in NCX expression/activity, associated with an increase in Ca2+ efflux from the cell, constitutes a primary alteration of Ca2+ -handling proteins in the evolution to HF. 3. No changes in SERCA2a expression/activity are observed when HF signs become evident.
Fil: Rodriguez, Jesica S.. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Velez Rueda, Jorge Omar. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Salas, Margarita. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Becerra, Romina Valeria. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina
Fil: Di Carlo, Mariano Nahuel. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Said, Maria Matilde. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Vittone, Leticia Beatriz. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Rinaldi, Gustavo Juan. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Portiansky, Enrique Leo. Universidad Nacional de la Plata. Facultad de Ciencias Veterinarias; Argentina
Fil: Mundiña, Cecilia Beatriz. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Palomeque, Julieta. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Mattiazzi, Ramona Alicia. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Materia
CALCIO
CALCIUM HANDLING PROTEINS
APOPTOSIS
HYPERTENSIVE DISEASE
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/12021
Acceder
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network_name_str CONICET Digital (CONICET)
spelling Increased Na+ /Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive ratsRodriguez, Jesica S.Velez Rueda, Jorge OmarSalas, MargaritaBecerra, Romina ValeriaDi Carlo, Mariano NahuelSaid, Maria MatildeVittone, Leticia BeatrizRinaldi, Gustavo JuanPortiansky, Enrique LeoMundiña, Cecilia BeatrizPalomeque, JulietaMattiazzi, Ramona AliciaCALCIOCALCIUM HANDLING PROTEINSAPOPTOSISHYPERTENSIVE DISEASEhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Spontaneously hypertensive rat (SHR) constitutes a genetic model widely used to study the natural evolution of hypertensive heart disease. Ca2+ -handling alterations are known to occur in SHR. However, the putative modifications of Ca2+ -handling proteins during the progression to heart failure (HF) are not well established. Moreover, the role of apoptosis in SHR is controversial. We investigated intracellular Ca2+ , Ca2+ -handling proteins and apoptosis in SHR vs. control Wistar rats (W) from 3 to 15 months (mo). Changes associated with the transition to HF (i.e. lung edema and decrease in midwall fractional shortening), occurred at 15 mo in 38% of SHR (SHRF). In SHRF, twitch and caffeine-induced Ca2+ transients, significantly decreased relative to 6/9 mo and 15 mo without HF signs. This decrease occurred in association with a decrease in the time constant of caffeine-Ca2+ transient decay and an increase in Na+ /Ca2+ exchanger (NCX) abundance (p, 0.05) with no changes in SERCA2a expression/activity. An increased Ca2+ -calmodulin-kinase II activity, associated with an enhancement of apoptosis (TUNEL and Bax/Bcl2) was observed in SHR relative to W from 3 to 15 mo. Conclusions: 1. Apoptosis is an early and persistent event that may contribute to hypertrophic remodeling but would not participate in the contractile impairment of SHRF. 2. The increase in NCX expression/activity, associated with an increase in Ca2+ efflux from the cell, constitutes a primary alteration of Ca2+ -handling proteins in the evolution to HF. 3. No changes in SERCA2a expression/activity are observed when HF signs become evident.Fil: Rodriguez, Jesica S.. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; ArgentinaFil: Velez Rueda, Jorge Omar. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; ArgentinaFil: Salas, Margarita. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; ArgentinaFil: Becerra, Romina Valeria. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; ArgentinaFil: Di Carlo, Mariano Nahuel. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; ArgentinaFil: Said, Maria Matilde. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; ArgentinaFil: Vittone, Leticia Beatriz. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; ArgentinaFil: Rinaldi, Gustavo Juan. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; ArgentinaFil: Portiansky, Enrique Leo. Universidad Nacional de la Plata. Facultad de Ciencias Veterinarias; ArgentinaFil: Mundiña, Cecilia Beatriz. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; ArgentinaFil: Palomeque, Julieta. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; ArgentinaFil: Mattiazzi, Ramona Alicia. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; ArgentinaPublic Library Of Science2014-04info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/12021Rodriguez, Jesica S.; Velez Rueda, Jorge Omar; Salas, Margarita; Becerra, Romina Valeria; Di Carlo, Mariano Nahuel; et al.; Increased Na+ /Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats; Public Library Of Science; Plos One; 9; 4; 4-2014; 1-10; e964001932-6203enginfo:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0096400info:eu-repo/semantics/altIdentifier/url/http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0096400info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4004550/info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:38:07Zoai:ri.conicet.gov.ar:11336/12021instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:38:07.974CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Increased Na+ /Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats
title Increased Na+ /Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats
spellingShingle Increased Na+ /Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats
Rodriguez, Jesica S.
CALCIO
CALCIUM HANDLING PROTEINS
APOPTOSIS
HYPERTENSIVE DISEASE
title_short Increased Na+ /Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats
title_full Increased Na+ /Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats
title_fullStr Increased Na+ /Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats
title_full_unstemmed Increased Na+ /Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats
title_sort Increased Na+ /Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats
dc.creator.none.fl_str_mv Rodriguez, Jesica S.
Velez Rueda, Jorge Omar
Salas, Margarita
Becerra, Romina Valeria
Di Carlo, Mariano Nahuel
Said, Maria Matilde
Vittone, Leticia Beatriz
Rinaldi, Gustavo Juan
Portiansky, Enrique Leo
Mundiña, Cecilia Beatriz
Palomeque, Julieta
Mattiazzi, Ramona Alicia
author Rodriguez, Jesica S.
author_facet Rodriguez, Jesica S.
Velez Rueda, Jorge Omar
Salas, Margarita
Becerra, Romina Valeria
Di Carlo, Mariano Nahuel
Said, Maria Matilde
Vittone, Leticia Beatriz
Rinaldi, Gustavo Juan
Portiansky, Enrique Leo
Mundiña, Cecilia Beatriz
Palomeque, Julieta
Mattiazzi, Ramona Alicia
author_role author
author2 Velez Rueda, Jorge Omar
Salas, Margarita
Becerra, Romina Valeria
Di Carlo, Mariano Nahuel
Said, Maria Matilde
Vittone, Leticia Beatriz
Rinaldi, Gustavo Juan
Portiansky, Enrique Leo
Mundiña, Cecilia Beatriz
Palomeque, Julieta
Mattiazzi, Ramona Alicia
author2_role author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv CALCIO
CALCIUM HANDLING PROTEINS
APOPTOSIS
HYPERTENSIVE DISEASE
topic CALCIO
CALCIUM HANDLING PROTEINS
APOPTOSIS
HYPERTENSIVE DISEASE
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Spontaneously hypertensive rat (SHR) constitutes a genetic model widely used to study the natural evolution of hypertensive heart disease. Ca2+ -handling alterations are known to occur in SHR. However, the putative modifications of Ca2+ -handling proteins during the progression to heart failure (HF) are not well established. Moreover, the role of apoptosis in SHR is controversial. We investigated intracellular Ca2+ , Ca2+ -handling proteins and apoptosis in SHR vs. control Wistar rats (W) from 3 to 15 months (mo). Changes associated with the transition to HF (i.e. lung edema and decrease in midwall fractional shortening), occurred at 15 mo in 38% of SHR (SHRF). In SHRF, twitch and caffeine-induced Ca2+ transients, significantly decreased relative to 6/9 mo and 15 mo without HF signs. This decrease occurred in association with a decrease in the time constant of caffeine-Ca2+ transient decay and an increase in Na+ /Ca2+ exchanger (NCX) abundance (p, 0.05) with no changes in SERCA2a expression/activity. An increased Ca2+ -calmodulin-kinase II activity, associated with an enhancement of apoptosis (TUNEL and Bax/Bcl2) was observed in SHR relative to W from 3 to 15 mo. Conclusions: 1. Apoptosis is an early and persistent event that may contribute to hypertrophic remodeling but would not participate in the contractile impairment of SHRF. 2. The increase in NCX expression/activity, associated with an increase in Ca2+ efflux from the cell, constitutes a primary alteration of Ca2+ -handling proteins in the evolution to HF. 3. No changes in SERCA2a expression/activity are observed when HF signs become evident.
Fil: Rodriguez, Jesica S.. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Velez Rueda, Jorge Omar. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Salas, Margarita. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Becerra, Romina Valeria. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina
Fil: Di Carlo, Mariano Nahuel. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Said, Maria Matilde. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Vittone, Leticia Beatriz. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Rinaldi, Gustavo Juan. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Portiansky, Enrique Leo. Universidad Nacional de la Plata. Facultad de Ciencias Veterinarias; Argentina
Fil: Mundiña, Cecilia Beatriz. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Palomeque, Julieta. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Mattiazzi, Ramona Alicia. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
description Spontaneously hypertensive rat (SHR) constitutes a genetic model widely used to study the natural evolution of hypertensive heart disease. Ca2+ -handling alterations are known to occur in SHR. However, the putative modifications of Ca2+ -handling proteins during the progression to heart failure (HF) are not well established. Moreover, the role of apoptosis in SHR is controversial. We investigated intracellular Ca2+ , Ca2+ -handling proteins and apoptosis in SHR vs. control Wistar rats (W) from 3 to 15 months (mo). Changes associated with the transition to HF (i.e. lung edema and decrease in midwall fractional shortening), occurred at 15 mo in 38% of SHR (SHRF). In SHRF, twitch and caffeine-induced Ca2+ transients, significantly decreased relative to 6/9 mo and 15 mo without HF signs. This decrease occurred in association with a decrease in the time constant of caffeine-Ca2+ transient decay and an increase in Na+ /Ca2+ exchanger (NCX) abundance (p, 0.05) with no changes in SERCA2a expression/activity. An increased Ca2+ -calmodulin-kinase II activity, associated with an enhancement of apoptosis (TUNEL and Bax/Bcl2) was observed in SHR relative to W from 3 to 15 mo. Conclusions: 1. Apoptosis is an early and persistent event that may contribute to hypertrophic remodeling but would not participate in the contractile impairment of SHRF. 2. The increase in NCX expression/activity, associated with an increase in Ca2+ efflux from the cell, constitutes a primary alteration of Ca2+ -handling proteins in the evolution to HF. 3. No changes in SERCA2a expression/activity are observed when HF signs become evident.
publishDate 2014
dc.date.none.fl_str_mv 2014-04
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
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info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/12021
Rodriguez, Jesica S.; Velez Rueda, Jorge Omar; Salas, Margarita; Becerra, Romina Valeria; Di Carlo, Mariano Nahuel; et al.; Increased Na+ /Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats; Public Library Of Science; Plos One; 9; 4; 4-2014; 1-10; e96400
1932-6203
url http://hdl.handle.net/11336/12021
identifier_str_mv Rodriguez, Jesica S.; Velez Rueda, Jorge Omar; Salas, Margarita; Becerra, Romina Valeria; Di Carlo, Mariano Nahuel; et al.; Increased Na+ /Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats; Public Library Of Science; Plos One; 9; 4; 4-2014; 1-10; e96400
1932-6203
dc.language.none.fl_str_mv eng
language eng
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info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4004550/
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
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rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
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publisher.none.fl_str_mv Public Library Of Science
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