Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: Role of NO and mitoKATP

Autores
Fantinelli, Juliana Catalina; Pérez Nuñez, Ignacio Adrián; González Arbeláez, Luisa Fernanda; Schinella, Guillermo R.; Mosca, Susana Maria
Año de publicación
2013
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Background: The mitochondrial permeability transition pore (mPTP) plays an important role in ischemia–reperfusion in normotensive animals. Our study aims to define their participation in the ischemic preconditioning (IP) in hypertrophied hearts and to assess the role played by NO and mitochondrial ATP-dependent K channels (mitoKATP). Material and methods: Isolated hearts from spontaneously hypertensive rats (SHR) and age-matched normotensive rats Wistar Kyoto (WKY) were subjected to 35-min or 50-min global ischemia (GI) followed by 2-hour reperfusion (R). IP was induced by a single cycle of 5-min GI and 10-min R (IP1) or three cycles of 2-min GI and 5-min R (IP3) applied before to prolonged ischemia. L-NAME (NOS inhibitor) or 5-HD (mitoKATP blocker) to investigate the role played by NO and mitoKATP, respectively were administered. Infarct size (IS), myocardial function, reduced glutathione (GSH) — as marker of oxidative stress and MnSOD cytosolic activity — as an index of mPTP opening were determined. Results: IP1 significantly decreased the IS in WKY hearts at both ischemia duration times. In SHR, IP1 decreased the IS observed in GI35 but it did not modify that detected at 50-min GI, which was limited by IP3. IP preserved GSH content and decreased MnSOD cytosolic activity in both rat strains. These protective effects were annulled by L-NAME and 5-HD for both ischemic periods in SHR, whereas in WKY they were only effective for 50-min GI. Conclusion: Our data demonstrate that the cardioprotection achieved by ischemic preconditioning in hearts from SHR hearts involves an attenuation of mPTP opening NO and mitoKATP-mediated.
Fil: Fantinelli, Juliana Catalina. 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: Pérez Nuñez, Ignacio Adrián. 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: González Arbeláez, Luisa Fernanda. 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. Ministerio de Ciencia, Tecnología e Innovación Productiva. Agencia Nacional de Promoción Cientifíca y Tecnológica; Argentina
Fil: Schinella, Guillermo R.. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Mosca, Susana Maria. 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
Ischemic Preconditioning
Shr
Mptp
No
Mitokatp
Gsh
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/11955
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/11955
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: Role of NO and mitoKATPFantinelli, Juliana CatalinaPérez Nuñez, Ignacio AdriánGonzález Arbeláez, Luisa FernandaSchinella, Guillermo R.Mosca, Susana MariaIschemic PreconditioningShrMptpNoMitokatpGshhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Background: The mitochondrial permeability transition pore (mPTP) plays an important role in ischemia–reperfusion in normotensive animals. Our study aims to define their participation in the ischemic preconditioning (IP) in hypertrophied hearts and to assess the role played by NO and mitochondrial ATP-dependent K channels (mitoKATP). Material and methods: Isolated hearts from spontaneously hypertensive rats (SHR) and age-matched normotensive rats Wistar Kyoto (WKY) were subjected to 35-min or 50-min global ischemia (GI) followed by 2-hour reperfusion (R). IP was induced by a single cycle of 5-min GI and 10-min R (IP1) or three cycles of 2-min GI and 5-min R (IP3) applied before to prolonged ischemia. L-NAME (NOS inhibitor) or 5-HD (mitoKATP blocker) to investigate the role played by NO and mitoKATP, respectively were administered. Infarct size (IS), myocardial function, reduced glutathione (GSH) — as marker of oxidative stress and MnSOD cytosolic activity — as an index of mPTP opening were determined. Results: IP1 significantly decreased the IS in WKY hearts at both ischemia duration times. In SHR, IP1 decreased the IS observed in GI35 but it did not modify that detected at 50-min GI, which was limited by IP3. IP preserved GSH content and decreased MnSOD cytosolic activity in both rat strains. These protective effects were annulled by L-NAME and 5-HD for both ischemic periods in SHR, whereas in WKY they were only effective for 50-min GI. Conclusion: Our data demonstrate that the cardioprotection achieved by ischemic preconditioning in hearts from SHR hearts involves an attenuation of mPTP opening NO and mitoKATP-mediated.Fil: Fantinelli, Juliana Catalina. 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: Pérez Nuñez, Ignacio Adrián. 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: González Arbeláez, Luisa Fernanda. 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. Ministerio de Ciencia, Tecnología e Innovación Productiva. Agencia Nacional de Promoción Cientifíca y Tecnológica; ArgentinaFil: Schinella, Guillermo R.. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; ArgentinaFil: Mosca, Susana Maria. 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; ArgentinaElsevier Ireland2013-06info: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/11336/11955Fantinelli, Juliana Catalina; Pérez Nuñez, Ignacio Adrián; González Arbeláez, Luisa Fernanda; Schinella, Guillermo R.; Mosca, Susana Maria; Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: Role of NO and mitoKATP; Elsevier Ireland; International Journal Of Cardiology; 166; 1; 6-2013; 173-1800167-5273enginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.ijcard.2011.10.103info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0167527311019772info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:09:37Zoai:ri.conicet.gov.ar:11336/11955instacron: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 10:09:37.7CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: Role of NO and mitoKATP
title Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: Role of NO and mitoKATP
spellingShingle Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: Role of NO and mitoKATP
Fantinelli, Juliana Catalina
Ischemic Preconditioning
Shr
Mptp
No
Mitokatp
Gsh
title_short Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: Role of NO and mitoKATP
title_full Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: Role of NO and mitoKATP
title_fullStr Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: Role of NO and mitoKATP
title_full_unstemmed Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: Role of NO and mitoKATP
title_sort Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: Role of NO and mitoKATP
dc.creator.none.fl_str_mv Fantinelli, Juliana Catalina
Pérez Nuñez, Ignacio Adrián
González Arbeláez, Luisa Fernanda
Schinella, Guillermo R.
Mosca, Susana Maria
author Fantinelli, Juliana Catalina
author_facet Fantinelli, Juliana Catalina
Pérez Nuñez, Ignacio Adrián
González Arbeláez, Luisa Fernanda
Schinella, Guillermo R.
Mosca, Susana Maria
author_role author
author2 Pérez Nuñez, Ignacio Adrián
González Arbeláez, Luisa Fernanda
Schinella, Guillermo R.
Mosca, Susana Maria
author2_role author
author
author
author
dc.subject.none.fl_str_mv Ischemic Preconditioning
Shr
Mptp
No
Mitokatp
Gsh
topic Ischemic Preconditioning
Shr
Mptp
No
Mitokatp
Gsh
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Background: The mitochondrial permeability transition pore (mPTP) plays an important role in ischemia–reperfusion in normotensive animals. Our study aims to define their participation in the ischemic preconditioning (IP) in hypertrophied hearts and to assess the role played by NO and mitochondrial ATP-dependent K channels (mitoKATP). Material and methods: Isolated hearts from spontaneously hypertensive rats (SHR) and age-matched normotensive rats Wistar Kyoto (WKY) were subjected to 35-min or 50-min global ischemia (GI) followed by 2-hour reperfusion (R). IP was induced by a single cycle of 5-min GI and 10-min R (IP1) or three cycles of 2-min GI and 5-min R (IP3) applied before to prolonged ischemia. L-NAME (NOS inhibitor) or 5-HD (mitoKATP blocker) to investigate the role played by NO and mitoKATP, respectively were administered. Infarct size (IS), myocardial function, reduced glutathione (GSH) — as marker of oxidative stress and MnSOD cytosolic activity — as an index of mPTP opening were determined. Results: IP1 significantly decreased the IS in WKY hearts at both ischemia duration times. In SHR, IP1 decreased the IS observed in GI35 but it did not modify that detected at 50-min GI, which was limited by IP3. IP preserved GSH content and decreased MnSOD cytosolic activity in both rat strains. These protective effects were annulled by L-NAME and 5-HD for both ischemic periods in SHR, whereas in WKY they were only effective for 50-min GI. Conclusion: Our data demonstrate that the cardioprotection achieved by ischemic preconditioning in hearts from SHR hearts involves an attenuation of mPTP opening NO and mitoKATP-mediated.
Fil: Fantinelli, Juliana Catalina. 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: Pérez Nuñez, Ignacio Adrián. 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: González Arbeláez, Luisa Fernanda. 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. Ministerio de Ciencia, Tecnología e Innovación Productiva. Agencia Nacional de Promoción Cientifíca y Tecnológica; Argentina
Fil: Schinella, Guillermo R.. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Mosca, Susana Maria. 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 Background: The mitochondrial permeability transition pore (mPTP) plays an important role in ischemia–reperfusion in normotensive animals. Our study aims to define their participation in the ischemic preconditioning (IP) in hypertrophied hearts and to assess the role played by NO and mitochondrial ATP-dependent K channels (mitoKATP). Material and methods: Isolated hearts from spontaneously hypertensive rats (SHR) and age-matched normotensive rats Wistar Kyoto (WKY) were subjected to 35-min or 50-min global ischemia (GI) followed by 2-hour reperfusion (R). IP was induced by a single cycle of 5-min GI and 10-min R (IP1) or three cycles of 2-min GI and 5-min R (IP3) applied before to prolonged ischemia. L-NAME (NOS inhibitor) or 5-HD (mitoKATP blocker) to investigate the role played by NO and mitoKATP, respectively were administered. Infarct size (IS), myocardial function, reduced glutathione (GSH) — as marker of oxidative stress and MnSOD cytosolic activity — as an index of mPTP opening were determined. Results: IP1 significantly decreased the IS in WKY hearts at both ischemia duration times. In SHR, IP1 decreased the IS observed in GI35 but it did not modify that detected at 50-min GI, which was limited by IP3. IP preserved GSH content and decreased MnSOD cytosolic activity in both rat strains. These protective effects were annulled by L-NAME and 5-HD for both ischemic periods in SHR, whereas in WKY they were only effective for 50-min GI. Conclusion: Our data demonstrate that the cardioprotection achieved by ischemic preconditioning in hearts from SHR hearts involves an attenuation of mPTP opening NO and mitoKATP-mediated.
publishDate 2013
dc.date.none.fl_str_mv 2013-06
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/11336/11955
Fantinelli, Juliana Catalina; Pérez Nuñez, Ignacio Adrián; González Arbeláez, Luisa Fernanda; Schinella, Guillermo R.; Mosca, Susana Maria; Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: Role of NO and mitoKATP; Elsevier Ireland; International Journal Of Cardiology; 166; 1; 6-2013; 173-180
0167-5273
url http://hdl.handle.net/11336/11955
identifier_str_mv Fantinelli, Juliana Catalina; Pérez Nuñez, Ignacio Adrián; González Arbeláez, Luisa Fernanda; Schinella, Guillermo R.; Mosca, Susana Maria; Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: Role of NO and mitoKATP; Elsevier Ireland; International Journal Of Cardiology; 166; 1; 6-2013; 173-180
0167-5273
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.ijcard.2011.10.103
info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0167527311019772
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Ireland
publisher.none.fl_str_mv Elsevier Ireland
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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