Mitochondrial reactive oxygen species activate the slow force response to stretch in feline myocardium

Autores
Caldiz, Claudia Irma; Garciarena, Carolina Denis; Dulce, Raúl Ariel; Novaretto, Leonardo P.; Yeves, Alejandra del Milagro; Ennis, Irene Lucía; Cingolani, Horacio Eugenio; Chiappe de Cingolani, Gladys Ethel; Pérez, Néstor Gustavo
Año de publicación
2007
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
When the length of the myocardium is increased, a biphasic response to stretch occurs involving an initial rapid increase in force followed by a delayed slow increase called the slow force response (SFR). Confirming previous findings involving angiotensin II in the SFR, it was blunted by AT1 receptor blockade (losartan). The SFR was accompanied by an increase in reactive oxygen species (ROS) of ∼30% and in intracellular Na+ concentration ([Na⁺]i) of ∼2.5 mmol l⁻¹ over basal detected by H2DCFDA and SBFI fluorescence, respectively. Abolition of ROS by 2-mercapto-propionyl-glycine (MPG) and EUK8 suppressed the increase in [Na⁺]i and the SFR, which were also blunted by Na⁺/H⁺ exchanger (NHE-1) inhibition (HOE642). NADPH oxidase inhibition (apocynin or DPI) or blockade of the ATP-sensitive mitochondrial potassium channels (5HD or glybenclamide) suppressed both the SFR and the increase in [Na⁺]i after stretch, suggesting that endogenous angiotensin II activated NADPH oxidase leading to ROS release by the ATP-sensitive mitochondrial potassium channels, which promoted NHE-1 activation. Supporting the notion of ROS-mediated NHE-1 activation, stretch increased the ERK1/2 and p90rsk kinases phosphorylation, effect that was cancelled by losartan. In agreement, the SFR was cancelled by inhibiting the ERK1/2 signalling pathway with PD98059. Angiotensin II at a dose that mimics the SFR (1 nmol l⁻¹) induced an increase in ·O₂− production of ∼30–40% detected by lucigenin in cardiac slices, an effect that was blunted by losartan, MPG, apocynin, 5HD and glybenclamide. Taken together the data suggest a pivotal role of mitochondrial ROS in the genesis of the SFR to stretch.
Centro de Investigaciones Cardiovasculares
Materia
Ciencias Médicas
Internal medicine
Endocrinology
Chemistry
Apocynin
Mitochondrial ROS
NADPH oxidase
Losartan
Angiotensin II
Reactive oxygen species
Intracellular
Potassium channel
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:10915/127168

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oai_identifier_str oai:sedici.unlp.edu.ar:10915/127168
network_acronym_str SEDICI
repository_id_str 1329
network_name_str SEDICI (UNLP)
spelling Mitochondrial reactive oxygen species activate the slow force response to stretch in feline myocardiumCaldiz, Claudia IrmaGarciarena, Carolina DenisDulce, Raúl ArielNovaretto, Leonardo P.Yeves, Alejandra del MilagroEnnis, Irene LucíaCingolani, Horacio EugenioChiappe de Cingolani, Gladys EthelPérez, Néstor GustavoCiencias MédicasInternal medicineEndocrinologyChemistryApocyninMitochondrial ROSNADPH oxidaseLosartanAngiotensin IIReactive oxygen speciesIntracellularPotassium channelWhen the length of the myocardium is increased, a biphasic response to stretch occurs involving an initial rapid increase in force followed by a delayed slow increase called the slow force response (SFR). Confirming previous findings involving angiotensin II in the SFR, it was blunted by AT1 receptor blockade (losartan). The SFR was accompanied by an increase in reactive oxygen species (ROS) of ∼30% and in intracellular Na+ concentration ([Na⁺]i) of ∼2.5 mmol l⁻¹ over basal detected by H2DCFDA and SBFI fluorescence, respectively. Abolition of ROS by 2-mercapto-propionyl-glycine (MPG) and EUK8 suppressed the increase in [Na⁺]i and the SFR, which were also blunted by Na⁺/H⁺ exchanger (NHE-1) inhibition (HOE642). NADPH oxidase inhibition (apocynin or DPI) or blockade of the ATP-sensitive mitochondrial potassium channels (5HD or glybenclamide) suppressed both the SFR and the increase in [Na⁺]i after stretch, suggesting that endogenous angiotensin II activated NADPH oxidase leading to ROS release by the ATP-sensitive mitochondrial potassium channels, which promoted NHE-1 activation. Supporting the notion of ROS-mediated NHE-1 activation, stretch increased the ERK1/2 and p90rsk kinases phosphorylation, effect that was cancelled by losartan. In agreement, the SFR was cancelled by inhibiting the ERK1/2 signalling pathway with PD98059. Angiotensin II at a dose that mimics the SFR (1 nmol l⁻¹) induced an increase in ·O₂− production of ∼30–40% detected by lucigenin in cardiac slices, an effect that was blunted by losartan, MPG, apocynin, 5HD and glybenclamide. Taken together the data suggest a pivotal role of mitochondrial ROS in the genesis of the SFR to stretch.Centro de Investigaciones Cardiovasculares2007-10-31info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf895-905http://sedici.unlp.edu.ar/handle/10915/127168enginfo:eu-repo/semantics/altIdentifier/issn/0022-3751info:eu-repo/semantics/altIdentifier/issn/1469-7793info:eu-repo/semantics/altIdentifier/doi/10.1113/jphysiol.2007.141689info: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:UNLP2025-09-29T11:30:42Zoai:sedici.unlp.edu.ar:10915/127168Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:30:43.218SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Mitochondrial reactive oxygen species activate the slow force response to stretch in feline myocardium
title Mitochondrial reactive oxygen species activate the slow force response to stretch in feline myocardium
spellingShingle Mitochondrial reactive oxygen species activate the slow force response to stretch in feline myocardium
Caldiz, Claudia Irma
Ciencias Médicas
Internal medicine
Endocrinology
Chemistry
Apocynin
Mitochondrial ROS
NADPH oxidase
Losartan
Angiotensin II
Reactive oxygen species
Intracellular
Potassium channel
title_short Mitochondrial reactive oxygen species activate the slow force response to stretch in feline myocardium
title_full Mitochondrial reactive oxygen species activate the slow force response to stretch in feline myocardium
title_fullStr Mitochondrial reactive oxygen species activate the slow force response to stretch in feline myocardium
title_full_unstemmed Mitochondrial reactive oxygen species activate the slow force response to stretch in feline myocardium
title_sort Mitochondrial reactive oxygen species activate the slow force response to stretch in feline myocardium
dc.creator.none.fl_str_mv Caldiz, Claudia Irma
Garciarena, Carolina Denis
Dulce, Raúl Ariel
Novaretto, Leonardo P.
Yeves, Alejandra del Milagro
Ennis, Irene Lucía
Cingolani, Horacio Eugenio
Chiappe de Cingolani, Gladys Ethel
Pérez, Néstor Gustavo
author Caldiz, Claudia Irma
author_facet Caldiz, Claudia Irma
Garciarena, Carolina Denis
Dulce, Raúl Ariel
Novaretto, Leonardo P.
Yeves, Alejandra del Milagro
Ennis, Irene Lucía
Cingolani, Horacio Eugenio
Chiappe de Cingolani, Gladys Ethel
Pérez, Néstor Gustavo
author_role author
author2 Garciarena, Carolina Denis
Dulce, Raúl Ariel
Novaretto, Leonardo P.
Yeves, Alejandra del Milagro
Ennis, Irene Lucía
Cingolani, Horacio Eugenio
Chiappe de Cingolani, Gladys Ethel
Pérez, Néstor Gustavo
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Ciencias Médicas
Internal medicine
Endocrinology
Chemistry
Apocynin
Mitochondrial ROS
NADPH oxidase
Losartan
Angiotensin II
Reactive oxygen species
Intracellular
Potassium channel
topic Ciencias Médicas
Internal medicine
Endocrinology
Chemistry
Apocynin
Mitochondrial ROS
NADPH oxidase
Losartan
Angiotensin II
Reactive oxygen species
Intracellular
Potassium channel
dc.description.none.fl_txt_mv When the length of the myocardium is increased, a biphasic response to stretch occurs involving an initial rapid increase in force followed by a delayed slow increase called the slow force response (SFR). Confirming previous findings involving angiotensin II in the SFR, it was blunted by AT1 receptor blockade (losartan). The SFR was accompanied by an increase in reactive oxygen species (ROS) of ∼30% and in intracellular Na+ concentration ([Na⁺]i) of ∼2.5 mmol l⁻¹ over basal detected by H2DCFDA and SBFI fluorescence, respectively. Abolition of ROS by 2-mercapto-propionyl-glycine (MPG) and EUK8 suppressed the increase in [Na⁺]i and the SFR, which were also blunted by Na⁺/H⁺ exchanger (NHE-1) inhibition (HOE642). NADPH oxidase inhibition (apocynin or DPI) or blockade of the ATP-sensitive mitochondrial potassium channels (5HD or glybenclamide) suppressed both the SFR and the increase in [Na⁺]i after stretch, suggesting that endogenous angiotensin II activated NADPH oxidase leading to ROS release by the ATP-sensitive mitochondrial potassium channels, which promoted NHE-1 activation. Supporting the notion of ROS-mediated NHE-1 activation, stretch increased the ERK1/2 and p90rsk kinases phosphorylation, effect that was cancelled by losartan. In agreement, the SFR was cancelled by inhibiting the ERK1/2 signalling pathway with PD98059. Angiotensin II at a dose that mimics the SFR (1 nmol l⁻¹) induced an increase in ·O₂− production of ∼30–40% detected by lucigenin in cardiac slices, an effect that was blunted by losartan, MPG, apocynin, 5HD and glybenclamide. Taken together the data suggest a pivotal role of mitochondrial ROS in the genesis of the SFR to stretch.
Centro de Investigaciones Cardiovasculares
description When the length of the myocardium is increased, a biphasic response to stretch occurs involving an initial rapid increase in force followed by a delayed slow increase called the slow force response (SFR). Confirming previous findings involving angiotensin II in the SFR, it was blunted by AT1 receptor blockade (losartan). The SFR was accompanied by an increase in reactive oxygen species (ROS) of ∼30% and in intracellular Na+ concentration ([Na⁺]i) of ∼2.5 mmol l⁻¹ over basal detected by H2DCFDA and SBFI fluorescence, respectively. Abolition of ROS by 2-mercapto-propionyl-glycine (MPG) and EUK8 suppressed the increase in [Na⁺]i and the SFR, which were also blunted by Na⁺/H⁺ exchanger (NHE-1) inhibition (HOE642). NADPH oxidase inhibition (apocynin or DPI) or blockade of the ATP-sensitive mitochondrial potassium channels (5HD or glybenclamide) suppressed both the SFR and the increase in [Na⁺]i after stretch, suggesting that endogenous angiotensin II activated NADPH oxidase leading to ROS release by the ATP-sensitive mitochondrial potassium channels, which promoted NHE-1 activation. Supporting the notion of ROS-mediated NHE-1 activation, stretch increased the ERK1/2 and p90rsk kinases phosphorylation, effect that was cancelled by losartan. In agreement, the SFR was cancelled by inhibiting the ERK1/2 signalling pathway with PD98059. Angiotensin II at a dose that mimics the SFR (1 nmol l⁻¹) induced an increase in ·O₂− production of ∼30–40% detected by lucigenin in cardiac slices, an effect that was blunted by losartan, MPG, apocynin, 5HD and glybenclamide. Taken together the data suggest a pivotal role of mitochondrial ROS in the genesis of the SFR to stretch.
publishDate 2007
dc.date.none.fl_str_mv 2007-10-31
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
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status_str publishedVersion
dc.identifier.none.fl_str_mv http://sedici.unlp.edu.ar/handle/10915/127168
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dc.language.none.fl_str_mv eng
language eng
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info:eu-repo/semantics/altIdentifier/issn/1469-7793
info:eu-repo/semantics/altIdentifier/doi/10.1113/jphysiol.2007.141689
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
895-905
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