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
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/127168
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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 Articulo 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://sedici.unlp.edu.ar/handle/10915/127168 |
url |
http://sedici.unlp.edu.ar/handle/10915/127168 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/issn/0022-3751 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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SEDICI (UNLP) - Universidad Nacional de La Plata |
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