Angiotensin II inhibits the electrogenic Na+/HCO3- cotransport of cat cardiac myocytes

Autores
de Giusti, Verónica Celeste; Orlowski, Alejandro; Aiello, Ernesto Alejandro
Año de publicación
2010
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The Na+/HCO3- cotransporter (NBC) plays an important role in intracellular pH (pHi) regulation in the heart. In the myocardium co-exist the electrogenic (eNBC) and electroneutral (nNBC) isoforms of NBC. We have recently reported that angiotensin II (Ang II) stimulated total NBC activity during the recovery from intracellular acidosis through a reactive oxygen species (ROS) and ERK-dependent pathway. In the present work we focus our attention on eNBC. In order to study the activity of the eNBC in isolation, we induced a membrane potential depolarization by increasing extracellular K+ [K+]o from 4.5 to 45mM (K+ pulse). This experimental protocol enhanced eNBC driving force leading to intracellular alkalization (0.19±0.008, n=6; data expressed as an increase of pHi units after 14min of applying the K+ pulse). This alkalization was completely abrogated by the NBC blocker S0859 (-0.004±0.016*, n=5; * indicates p<0.05 vs control) but not by the Na+/H+ exchanger blocker HOE642 (0.185±0.04, n=4), indicating that we are exclusively measuring eNBC. The K+ pulse induced alkalization was canceled by 100nM Ang II (-0.008±0.018*; n=5). This inhibitory effect was prevented when the myocytes were incubated with losartan (AT1 receptor blocker, 0.18±0.02; n=4) or SB202190 (p38 MAP kinase inhibitor, 0.25±0.06; n=5). Neither chelerythrine (PKC inhibitor, -0.06±0.04*; n=4), nor U0126 (ERK inhibitor, -0.07±0.04*; n=4) nor MPG (ROS scavenger, -0.02±0.05*; n=8) affected the Ang II-induced inhibition of eNBC. The inhibitory action of Ang II on eNBC was corroborated with perforated patch-clamp experiments, since no impact of the current produced by eNBC on action potential repolarization was observed in the presence of Ang II. In conclusion, we propose that Ang II, binding to AT1 receptors, exerts an inhibitory effect on eNBC activity in a p38 kinase-dependent manner. © 2010 Elsevier Ltd.
Fil: de Giusti, Verónica Celeste. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Orlowski, Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Aiello, Ernesto Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Materia
Angiotensin Ii
Cardiac Myocytes
Erk 1/2 Kinase
Na+/Hco3- Co-Transporter
P38 Kinase
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/61764
Acceder
id CONICETDig_ee4099d9afa7196884a78eba37bad4ba
oai_identifier_str oai:ri.conicet.gov.ar:11336/61764
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Angiotensin II inhibits the electrogenic Na+/HCO3- cotransport of cat cardiac myocytesde Giusti, Verónica CelesteOrlowski, AlejandroAiello, Ernesto AlejandroAngiotensin IiCardiac MyocytesErk 1/2 KinaseNa+/Hco3- Co-TransporterP38 Kinasehttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3The Na+/HCO3- cotransporter (NBC) plays an important role in intracellular pH (pHi) regulation in the heart. In the myocardium co-exist the electrogenic (eNBC) and electroneutral (nNBC) isoforms of NBC. We have recently reported that angiotensin II (Ang II) stimulated total NBC activity during the recovery from intracellular acidosis through a reactive oxygen species (ROS) and ERK-dependent pathway. In the present work we focus our attention on eNBC. In order to study the activity of the eNBC in isolation, we induced a membrane potential depolarization by increasing extracellular K+ [K+]o from 4.5 to 45mM (K+ pulse). This experimental protocol enhanced eNBC driving force leading to intracellular alkalization (0.19±0.008, n=6; data expressed as an increase of pHi units after 14min of applying the K+ pulse). This alkalization was completely abrogated by the NBC blocker S0859 (-0.004±0.016*, n=5; * indicates p<0.05 vs control) but not by the Na+/H+ exchanger blocker HOE642 (0.185±0.04, n=4), indicating that we are exclusively measuring eNBC. The K+ pulse induced alkalization was canceled by 100nM Ang II (-0.008±0.018*; n=5). This inhibitory effect was prevented when the myocytes were incubated with losartan (AT1 receptor blocker, 0.18±0.02; n=4) or SB202190 (p38 MAP kinase inhibitor, 0.25±0.06; n=5). Neither chelerythrine (PKC inhibitor, -0.06±0.04*; n=4), nor U0126 (ERK inhibitor, -0.07±0.04*; n=4) nor MPG (ROS scavenger, -0.02±0.05*; n=8) affected the Ang II-induced inhibition of eNBC. The inhibitory action of Ang II on eNBC was corroborated with perforated patch-clamp experiments, since no impact of the current produced by eNBC on action potential repolarization was observed in the presence of Ang II. In conclusion, we propose that Ang II, binding to AT1 receptors, exerts an inhibitory effect on eNBC activity in a p38 kinase-dependent manner. © 2010 Elsevier Ltd.Fil: de Giusti, Verónica Celeste. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: Orlowski, Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: Aiello, Ernesto Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaAcademic Press Ltd - Elsevier Science Ltd2010-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/61764de Giusti, Verónica Celeste; Orlowski, Alejandro; Aiello, Ernesto Alejandro; Angiotensin II inhibits the electrogenic Na+/HCO3- cotransport of cat cardiac myocytes; Academic Press Ltd - Elsevier Science Ltd; Journal of Molecular and Cellular Cardiology; 49; 5; 11-2010; 812-8180022-2828CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.yjmcc.2010.07.018info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S002228281000283Xinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:46:38Zoai:ri.conicet.gov.ar:11336/61764instacron: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:34982025-09-03 09:46:39.011CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Angiotensin II inhibits the electrogenic Na+/HCO3- cotransport of cat cardiac myocytes
title Angiotensin II inhibits the electrogenic Na+/HCO3- cotransport of cat cardiac myocytes
spellingShingle Angiotensin II inhibits the electrogenic Na+/HCO3- cotransport of cat cardiac myocytes
de Giusti, Verónica Celeste
Angiotensin Ii
Cardiac Myocytes
Erk 1/2 Kinase
Na+/Hco3- Co-Transporter
P38 Kinase
title_short Angiotensin II inhibits the electrogenic Na+/HCO3- cotransport of cat cardiac myocytes
title_full Angiotensin II inhibits the electrogenic Na+/HCO3- cotransport of cat cardiac myocytes
title_fullStr Angiotensin II inhibits the electrogenic Na+/HCO3- cotransport of cat cardiac myocytes
title_full_unstemmed Angiotensin II inhibits the electrogenic Na+/HCO3- cotransport of cat cardiac myocytes
title_sort Angiotensin II inhibits the electrogenic Na+/HCO3- cotransport of cat cardiac myocytes
dc.creator.none.fl_str_mv de Giusti, Verónica Celeste
Orlowski, Alejandro
Aiello, Ernesto Alejandro
author de Giusti, Verónica Celeste
author_facet de Giusti, Verónica Celeste
Orlowski, Alejandro
Aiello, Ernesto Alejandro
author_role author
author2 Orlowski, Alejandro
Aiello, Ernesto Alejandro
author2_role author
author
dc.subject.none.fl_str_mv Angiotensin Ii
Cardiac Myocytes
Erk 1/2 Kinase
Na+/Hco3- Co-Transporter
P38 Kinase
topic Angiotensin Ii
Cardiac Myocytes
Erk 1/2 Kinase
Na+/Hco3- Co-Transporter
P38 Kinase
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The Na+/HCO3- cotransporter (NBC) plays an important role in intracellular pH (pHi) regulation in the heart. In the myocardium co-exist the electrogenic (eNBC) and electroneutral (nNBC) isoforms of NBC. We have recently reported that angiotensin II (Ang II) stimulated total NBC activity during the recovery from intracellular acidosis through a reactive oxygen species (ROS) and ERK-dependent pathway. In the present work we focus our attention on eNBC. In order to study the activity of the eNBC in isolation, we induced a membrane potential depolarization by increasing extracellular K+ [K+]o from 4.5 to 45mM (K+ pulse). This experimental protocol enhanced eNBC driving force leading to intracellular alkalization (0.19±0.008, n=6; data expressed as an increase of pHi units after 14min of applying the K+ pulse). This alkalization was completely abrogated by the NBC blocker S0859 (-0.004±0.016*, n=5; * indicates p<0.05 vs control) but not by the Na+/H+ exchanger blocker HOE642 (0.185±0.04, n=4), indicating that we are exclusively measuring eNBC. The K+ pulse induced alkalization was canceled by 100nM Ang II (-0.008±0.018*; n=5). This inhibitory effect was prevented when the myocytes were incubated with losartan (AT1 receptor blocker, 0.18±0.02; n=4) or SB202190 (p38 MAP kinase inhibitor, 0.25±0.06; n=5). Neither chelerythrine (PKC inhibitor, -0.06±0.04*; n=4), nor U0126 (ERK inhibitor, -0.07±0.04*; n=4) nor MPG (ROS scavenger, -0.02±0.05*; n=8) affected the Ang II-induced inhibition of eNBC. The inhibitory action of Ang II on eNBC was corroborated with perforated patch-clamp experiments, since no impact of the current produced by eNBC on action potential repolarization was observed in the presence of Ang II. In conclusion, we propose that Ang II, binding to AT1 receptors, exerts an inhibitory effect on eNBC activity in a p38 kinase-dependent manner. © 2010 Elsevier Ltd.
Fil: de Giusti, Verónica Celeste. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Orlowski, Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Aiello, Ernesto Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
description The Na+/HCO3- cotransporter (NBC) plays an important role in intracellular pH (pHi) regulation in the heart. In the myocardium co-exist the electrogenic (eNBC) and electroneutral (nNBC) isoforms of NBC. We have recently reported that angiotensin II (Ang II) stimulated total NBC activity during the recovery from intracellular acidosis through a reactive oxygen species (ROS) and ERK-dependent pathway. In the present work we focus our attention on eNBC. In order to study the activity of the eNBC in isolation, we induced a membrane potential depolarization by increasing extracellular K+ [K+]o from 4.5 to 45mM (K+ pulse). This experimental protocol enhanced eNBC driving force leading to intracellular alkalization (0.19±0.008, n=6; data expressed as an increase of pHi units after 14min of applying the K+ pulse). This alkalization was completely abrogated by the NBC blocker S0859 (-0.004±0.016*, n=5; * indicates p<0.05 vs control) but not by the Na+/H+ exchanger blocker HOE642 (0.185±0.04, n=4), indicating that we are exclusively measuring eNBC. The K+ pulse induced alkalization was canceled by 100nM Ang II (-0.008±0.018*; n=5). This inhibitory effect was prevented when the myocytes were incubated with losartan (AT1 receptor blocker, 0.18±0.02; n=4) or SB202190 (p38 MAP kinase inhibitor, 0.25±0.06; n=5). Neither chelerythrine (PKC inhibitor, -0.06±0.04*; n=4), nor U0126 (ERK inhibitor, -0.07±0.04*; n=4) nor MPG (ROS scavenger, -0.02±0.05*; n=8) affected the Ang II-induced inhibition of eNBC. The inhibitory action of Ang II on eNBC was corroborated with perforated patch-clamp experiments, since no impact of the current produced by eNBC on action potential repolarization was observed in the presence of Ang II. In conclusion, we propose that Ang II, binding to AT1 receptors, exerts an inhibitory effect on eNBC activity in a p38 kinase-dependent manner. © 2010 Elsevier Ltd.
publishDate 2010
dc.date.none.fl_str_mv 2010-11
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/61764
de Giusti, Verónica Celeste; Orlowski, Alejandro; Aiello, Ernesto Alejandro; Angiotensin II inhibits the electrogenic Na+/HCO3- cotransport of cat cardiac myocytes; Academic Press Ltd - Elsevier Science Ltd; Journal of Molecular and Cellular Cardiology; 49; 5; 11-2010; 812-818
0022-2828
CONICET Digital
CONICET
url http://hdl.handle.net/11336/61764
identifier_str_mv de Giusti, Verónica Celeste; Orlowski, Alejandro; Aiello, Ernesto Alejandro; Angiotensin II inhibits the electrogenic Na+/HCO3- cotransport of cat cardiac myocytes; Academic Press Ltd - Elsevier Science Ltd; Journal of Molecular and Cellular Cardiology; 49; 5; 11-2010; 812-818
0022-2828
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.yjmcc.2010.07.018
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S002228281000283X
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Academic Press Ltd - Elsevier Science Ltd
publisher.none.fl_str_mv Academic Press Ltd - Elsevier Science Ltd
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.13397

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