Modulation of the cardiac sodium/bicarbonate cotransporter by the renin angiotensin aldosterone system: pathophysiological consequences

Autores
De Giusti, Verónica Celeste; Ciancio, María Carolina; Orlowski, Alejandro; Aiello, Ernesto Alejandro
Año de publicación
2014
Idioma
inglés
Tipo de recurso
reseña artículo
Estado
versión publicada
Descripción
The sodium/bicarbonate cotransporter (NBC) is one of the major alkalinizing mechanisms in the cardiomyocytes. It has been demonstrated the existence of at least two functional isoforms, one that promotes the co-influx of 1 molecule of Na+ per 1 molecule of HCO¯3 (electroneutral isoform; NBCn1) and the other one that generates the co-influx of 1 molecule of Na+ per 2 molecules of HCO¯3 (electrogenic isoform; NBCe1). Both isoforms are important to maintain intracellular pH (pHi) and sodium concentration ([Na+]i). In addition, NBCe1 generates an anionic repolarizing current that modulates the action potential duration (APD). The renin-angiotensin-aldosterone system (RAAS) is implicated in the modulation of almost all physiological cardiac functions and is also involved in the development and progression of cardiac diseases. It was reported that angiotensin II (Ang II) exhibits an opposite effect on NBC isoforms: it activates NBCn1 and inhibits NBCe1. The activation of NBCn1 leads to an increase in pHi and [Na+]i, which indirectly, due to the stimulation of reverse mode of the Na+/Ca2+ exchanger (NCX), conduces to an increase in the intracellular Ca2+ concentration. On the other hand, the inhibition of NBCe1 generates an APD prolongation, potentially representing a risk of arrhythmias. In the last years, the potentially altered NBC function in pathological scenarios, as cardiac hypertrophy and ischemia-reperfusion, has raised increasing interest among investigators. This review attempts to draw the attention on the relevant regulation of NBC activity by RAAS, since it modulates pHi and [Na+]i, which are involved in the development of cardiac hypertrophy, the damage produced by ischemia-reperfusion and the generation of arrhythmic events, suggesting a potential role of NBC in cardiac diseases.
Facultad de Ciencias Médicas
Centro de Investigaciones Cardiovasculares
Materia
Ciencias Médicas
Aldosterone
Angiotensin II
Heart
Hypertrophy
Sodium bicarbonate cotransporter
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:10915/85075

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spelling Modulation of the cardiac sodium/bicarbonate cotransporter by the renin angiotensin aldosterone system: pathophysiological consequencesDe Giusti, Verónica CelesteCiancio, María CarolinaOrlowski, AlejandroAiello, Ernesto AlejandroCiencias MédicasAldosteroneAngiotensin IIHeartHypertrophySodium bicarbonate cotransporterThe sodium/bicarbonate cotransporter (NBC) is one of the major alkalinizing mechanisms in the cardiomyocytes. It has been demonstrated the existence of at least two functional isoforms, one that promotes the co-influx of 1 molecule of Na<SUP>+</SUP> per 1 molecule of HCO¯<SUB>3</SUB> (electroneutral isoform; NBCn1) and the other one that generates the co-influx of 1 molecule of Na<SUP>+</SUP> per 2 molecules of HCO¯<SUB>3</SUB> (electrogenic isoform; NBCe1). Both isoforms are important to maintain intracellular pH (pH<SUB>i</SUB>) and sodium concentration ([Na<SUP>+</SUP>]<SUB>i</SUB>). In addition, NBCe1 generates an anionic repolarizing current that modulates the action potential duration (APD). The renin-angiotensin-aldosterone system (RAAS) is implicated in the modulation of almost all physiological cardiac functions and is also involved in the development and progression of cardiac diseases. It was reported that angiotensin II (Ang II) exhibits an opposite effect on NBC isoforms: it activates NBCn1 and inhibits NBCe1. The activation of NBCn1 leads to an increase in pH<SUB>i</SUB> and [Na<SUP>+</SUP>]<SUB>i</SUB>, which indirectly, due to the stimulation of reverse mode of the Na<SUP>+</SUP>/Ca<SUP>2+</SUP> exchanger (NCX), conduces to an increase in the intracellular Ca<SUP>2+</SUP> concentration. On the other hand, the inhibition of NBCe1 generates an APD prolongation, potentially representing a risk of arrhythmias. In the last years, the potentially altered NBC function in pathological scenarios, as cardiac hypertrophy and ischemia-reperfusion, has raised increasing interest among investigators. This review attempts to draw the attention on the relevant regulation of NBC activity by RAAS, since it modulates pH<SUB>i</SUB> and [Na<SUP>+</SUP>]<SUB>i</SUB>, which are involved in the development of cardiac hypertrophy, the damage produced by ischemia-reperfusion and the generation of arrhythmic events, suggesting a potential role of NBC in cardiac diseases.Facultad de Ciencias MédicasCentro de Investigaciones Cardiovasculares2014info: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/10915/85075enginfo:eu-repo/semantics/altIdentifier/issn/1664-042Xinfo:eu-repo/semantics/altIdentifier/doi/10.3389/fphys.2013.00411info: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:UNLP2025-09-03T10:48:41Zoai:sedici.unlp.edu.ar:10915/85075Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-03 10:48:41.35SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Modulation of the cardiac sodium/bicarbonate cotransporter by the renin angiotensin aldosterone system: pathophysiological consequences
title Modulation of the cardiac sodium/bicarbonate cotransporter by the renin angiotensin aldosterone system: pathophysiological consequences
spellingShingle Modulation of the cardiac sodium/bicarbonate cotransporter by the renin angiotensin aldosterone system: pathophysiological consequences
De Giusti, Verónica Celeste
Ciencias Médicas
Aldosterone
Angiotensin II
Heart
Hypertrophy
Sodium bicarbonate cotransporter
title_short Modulation of the cardiac sodium/bicarbonate cotransporter by the renin angiotensin aldosterone system: pathophysiological consequences
title_full Modulation of the cardiac sodium/bicarbonate cotransporter by the renin angiotensin aldosterone system: pathophysiological consequences
title_fullStr Modulation of the cardiac sodium/bicarbonate cotransporter by the renin angiotensin aldosterone system: pathophysiological consequences
title_full_unstemmed Modulation of the cardiac sodium/bicarbonate cotransporter by the renin angiotensin aldosterone system: pathophysiological consequences
title_sort Modulation of the cardiac sodium/bicarbonate cotransporter by the renin angiotensin aldosterone system: pathophysiological consequences
dc.creator.none.fl_str_mv De Giusti, Verónica Celeste
Ciancio, María Carolina
Orlowski, Alejandro
Aiello, Ernesto Alejandro
author De Giusti, Verónica Celeste
author_facet De Giusti, Verónica Celeste
Ciancio, María Carolina
Orlowski, Alejandro
Aiello, Ernesto Alejandro
author_role author
author2 Ciancio, María Carolina
Orlowski, Alejandro
Aiello, Ernesto Alejandro
author2_role author
author
author
dc.subject.none.fl_str_mv Ciencias Médicas
Aldosterone
Angiotensin II
Heart
Hypertrophy
Sodium bicarbonate cotransporter
topic Ciencias Médicas
Aldosterone
Angiotensin II
Heart
Hypertrophy
Sodium bicarbonate cotransporter
dc.description.none.fl_txt_mv The sodium/bicarbonate cotransporter (NBC) is one of the major alkalinizing mechanisms in the cardiomyocytes. It has been demonstrated the existence of at least two functional isoforms, one that promotes the co-influx of 1 molecule of Na<SUP>+</SUP> per 1 molecule of HCO¯<SUB>3</SUB> (electroneutral isoform; NBCn1) and the other one that generates the co-influx of 1 molecule of Na<SUP>+</SUP> per 2 molecules of HCO¯<SUB>3</SUB> (electrogenic isoform; NBCe1). Both isoforms are important to maintain intracellular pH (pH<SUB>i</SUB>) and sodium concentration ([Na<SUP>+</SUP>]<SUB>i</SUB>). In addition, NBCe1 generates an anionic repolarizing current that modulates the action potential duration (APD). The renin-angiotensin-aldosterone system (RAAS) is implicated in the modulation of almost all physiological cardiac functions and is also involved in the development and progression of cardiac diseases. It was reported that angiotensin II (Ang II) exhibits an opposite effect on NBC isoforms: it activates NBCn1 and inhibits NBCe1. The activation of NBCn1 leads to an increase in pH<SUB>i</SUB> and [Na<SUP>+</SUP>]<SUB>i</SUB>, which indirectly, due to the stimulation of reverse mode of the Na<SUP>+</SUP>/Ca<SUP>2+</SUP> exchanger (NCX), conduces to an increase in the intracellular Ca<SUP>2+</SUP> concentration. On the other hand, the inhibition of NBCe1 generates an APD prolongation, potentially representing a risk of arrhythmias. In the last years, the potentially altered NBC function in pathological scenarios, as cardiac hypertrophy and ischemia-reperfusion, has raised increasing interest among investigators. This review attempts to draw the attention on the relevant regulation of NBC activity by RAAS, since it modulates pH<SUB>i</SUB> and [Na<SUP>+</SUP>]<SUB>i</SUB>, which are involved in the development of cardiac hypertrophy, the damage produced by ischemia-reperfusion and the generation of arrhythmic events, suggesting a potential role of NBC in cardiac diseases.
Facultad de Ciencias Médicas
Centro de Investigaciones Cardiovasculares
description The sodium/bicarbonate cotransporter (NBC) is one of the major alkalinizing mechanisms in the cardiomyocytes. It has been demonstrated the existence of at least two functional isoforms, one that promotes the co-influx of 1 molecule of Na<SUP>+</SUP> per 1 molecule of HCO¯<SUB>3</SUB> (electroneutral isoform; NBCn1) and the other one that generates the co-influx of 1 molecule of Na<SUP>+</SUP> per 2 molecules of HCO¯<SUB>3</SUB> (electrogenic isoform; NBCe1). Both isoforms are important to maintain intracellular pH (pH<SUB>i</SUB>) and sodium concentration ([Na<SUP>+</SUP>]<SUB>i</SUB>). In addition, NBCe1 generates an anionic repolarizing current that modulates the action potential duration (APD). The renin-angiotensin-aldosterone system (RAAS) is implicated in the modulation of almost all physiological cardiac functions and is also involved in the development and progression of cardiac diseases. It was reported that angiotensin II (Ang II) exhibits an opposite effect on NBC isoforms: it activates NBCn1 and inhibits NBCe1. The activation of NBCn1 leads to an increase in pH<SUB>i</SUB> and [Na<SUP>+</SUP>]<SUB>i</SUB>, which indirectly, due to the stimulation of reverse mode of the Na<SUP>+</SUP>/Ca<SUP>2+</SUP> exchanger (NCX), conduces to an increase in the intracellular Ca<SUP>2+</SUP> concentration. On the other hand, the inhibition of NBCe1 generates an APD prolongation, potentially representing a risk of arrhythmias. In the last years, the potentially altered NBC function in pathological scenarios, as cardiac hypertrophy and ischemia-reperfusion, has raised increasing interest among investigators. This review attempts to draw the attention on the relevant regulation of NBC activity by RAAS, since it modulates pH<SUB>i</SUB> and [Na<SUP>+</SUP>]<SUB>i</SUB>, which are involved in the development of cardiac hypertrophy, the damage produced by ischemia-reperfusion and the generation of arrhythmic events, suggesting a potential role of NBC in cardiac diseases.
publishDate 2014
dc.date.none.fl_str_mv 2014
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info:eu-repo/semantics/altIdentifier/doi/10.3389/fphys.2013.00411
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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)
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