Reactive oxygen species partially mediate high dose angiotensin II-induced positive inotropic effect in cat ventricular myocytes
- Autores
- Yeves, Alejandra del Milagro; Caldiz, Claudia Irma; Aiello, Ernesto Alejandro; Villa Abrille, María Celeste; Ennis, Irene Lucía
- Año de publicación
- 2015
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Background: Reactive oxygen species, such as superoxide, are being increasingly recognized as key components of a vast array of signaling pathways. Angiotensin II is a well-recognized stimulus for superoxide production through NADPH oxidase activation and opening of the mitochondrial ATP-sensitive potassium channels (mKATP). A role for this mechanism has been proposed to explain several physiological effects of the peptide. The aim of this study was to evaluate the involvement of this mechanism in the inotropic response to 100 nmol/L angiotensin II. Methods: Sarcomere shortening and intracellular pH (BCECF-epifluorescence technique) were evaluated in isolated cat ventricular myocytes placed in a perfusion chamber on the stage of an inverted microscope. Myocardial superoxide production was evaluated by the lucigenin quimioluminiscence method. Results: Angiotensin II (100 nmol/L) increased~70% sarcomere shortening, effect that was only partially prevented by NADPH oxidase inhibition,mKATP channel blockade or inhibition of the cardiac Na+/H+ exchanger (NHE-1). Moreover, angiotensin II stimulates NHE-1 activity by a NADPH oxidase-dependent mechanism. Myocardial superoxide production was also increased by angiotensin II, and this action was completely prevented either by NADPH oxidase inhibition or mKATP channel blockade. Conclusions: The positive inotropic response to 100 nmol/L angiotensin II is due to both ROS/NHE-1 dependent and independent pathways, this being a point of divergence with the signaling previously described to be triggered by lower concentrations of angiotensin II (i.e.: 1 nmol/L).
Centro de Investigaciones Cardiovasculares - Materia
-
Medicina
Angiotensin II
Inotropism
Reactive oxygen species
NHE-1
Isolated cardiomyocytes - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by/4.0/
- Repositorio
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/114769
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Reactive oxygen species partially mediate high dose angiotensin II-induced positive inotropic effect in cat ventricular myocytesYeves, Alejandra del MilagroCaldiz, Claudia IrmaAiello, Ernesto AlejandroVilla Abrille, María CelesteEnnis, Irene LucíaMedicinaAngiotensin IIInotropismReactive oxygen speciesNHE-1Isolated cardiomyocytesBackground: Reactive oxygen species, such as superoxide, are being increasingly recognized as key components of a vast array of signaling pathways. Angiotensin II is a well-recognized stimulus for superoxide production through NADPH oxidase activation and opening of the mitochondrial ATP-sensitive potassium channels (mKATP). A role for this mechanism has been proposed to explain several physiological effects of the peptide. The aim of this study was to evaluate the involvement of this mechanism in the inotropic response to 100 nmol/L angiotensin II. Methods: Sarcomere shortening and intracellular pH (BCECF-epifluorescence technique) were evaluated in isolated cat ventricular myocytes placed in a perfusion chamber on the stage of an inverted microscope. Myocardial superoxide production was evaluated by the lucigenin quimioluminiscence method. Results: Angiotensin II (100 nmol/L) increased~70% sarcomere shortening, effect that was only partially prevented by NADPH oxidase inhibition,mKATP channel blockade or inhibition of the cardiac Na+/H+ exchanger (NHE-1). Moreover, angiotensin II stimulates NHE-1 activity by a NADPH oxidase-dependent mechanism. Myocardial superoxide production was also increased by angiotensin II, and this action was completely prevented either by NADPH oxidase inhibition or mKATP channel blockade. Conclusions: The positive inotropic response to 100 nmol/L angiotensin II is due to both ROS/NHE-1 dependent and independent pathways, this being a point of divergence with the signaling previously described to be triggered by lower concentrations of angiotensin II (i.e.: 1 nmol/L).Centro de Investigaciones Cardiovasculares2015info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf236-240http://sedici.unlp.edu.ar/handle/10915/114769enginfo:eu-repo/semantics/altIdentifier/issn/1054-8807info:eu-repo/semantics/altIdentifier/doi/10.1016/j.carpath.2015.01.002info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/Creative Commons Attribution 4.0 International (CC BY 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:26:44Zoai:sedici.unlp.edu.ar:10915/114769Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:26:44.781SEDICI (UNLP) - Universidad Nacional de La Platafalse |
dc.title.none.fl_str_mv |
Reactive oxygen species partially mediate high dose angiotensin II-induced positive inotropic effect in cat ventricular myocytes |
title |
Reactive oxygen species partially mediate high dose angiotensin II-induced positive inotropic effect in cat ventricular myocytes |
spellingShingle |
Reactive oxygen species partially mediate high dose angiotensin II-induced positive inotropic effect in cat ventricular myocytes Yeves, Alejandra del Milagro Medicina Angiotensin II Inotropism Reactive oxygen species NHE-1 Isolated cardiomyocytes |
title_short |
Reactive oxygen species partially mediate high dose angiotensin II-induced positive inotropic effect in cat ventricular myocytes |
title_full |
Reactive oxygen species partially mediate high dose angiotensin II-induced positive inotropic effect in cat ventricular myocytes |
title_fullStr |
Reactive oxygen species partially mediate high dose angiotensin II-induced positive inotropic effect in cat ventricular myocytes |
title_full_unstemmed |
Reactive oxygen species partially mediate high dose angiotensin II-induced positive inotropic effect in cat ventricular myocytes |
title_sort |
Reactive oxygen species partially mediate high dose angiotensin II-induced positive inotropic effect in cat ventricular myocytes |
dc.creator.none.fl_str_mv |
Yeves, Alejandra del Milagro Caldiz, Claudia Irma Aiello, Ernesto Alejandro Villa Abrille, María Celeste Ennis, Irene Lucía |
author |
Yeves, Alejandra del Milagro |
author_facet |
Yeves, Alejandra del Milagro Caldiz, Claudia Irma Aiello, Ernesto Alejandro Villa Abrille, María Celeste Ennis, Irene Lucía |
author_role |
author |
author2 |
Caldiz, Claudia Irma Aiello, Ernesto Alejandro Villa Abrille, María Celeste Ennis, Irene Lucía |
author2_role |
author author author author |
dc.subject.none.fl_str_mv |
Medicina Angiotensin II Inotropism Reactive oxygen species NHE-1 Isolated cardiomyocytes |
topic |
Medicina Angiotensin II Inotropism Reactive oxygen species NHE-1 Isolated cardiomyocytes |
dc.description.none.fl_txt_mv |
Background: Reactive oxygen species, such as superoxide, are being increasingly recognized as key components of a vast array of signaling pathways. Angiotensin II is a well-recognized stimulus for superoxide production through NADPH oxidase activation and opening of the mitochondrial ATP-sensitive potassium channels (mKATP). A role for this mechanism has been proposed to explain several physiological effects of the peptide. The aim of this study was to evaluate the involvement of this mechanism in the inotropic response to 100 nmol/L angiotensin II. Methods: Sarcomere shortening and intracellular pH (BCECF-epifluorescence technique) were evaluated in isolated cat ventricular myocytes placed in a perfusion chamber on the stage of an inverted microscope. Myocardial superoxide production was evaluated by the lucigenin quimioluminiscence method. Results: Angiotensin II (100 nmol/L) increased~70% sarcomere shortening, effect that was only partially prevented by NADPH oxidase inhibition,mKATP channel blockade or inhibition of the cardiac Na+/H+ exchanger (NHE-1). Moreover, angiotensin II stimulates NHE-1 activity by a NADPH oxidase-dependent mechanism. Myocardial superoxide production was also increased by angiotensin II, and this action was completely prevented either by NADPH oxidase inhibition or mKATP channel blockade. Conclusions: The positive inotropic response to 100 nmol/L angiotensin II is due to both ROS/NHE-1 dependent and independent pathways, this being a point of divergence with the signaling previously described to be triggered by lower concentrations of angiotensin II (i.e.: 1 nmol/L). Centro de Investigaciones Cardiovasculares |
description |
Background: Reactive oxygen species, such as superoxide, are being increasingly recognized as key components of a vast array of signaling pathways. Angiotensin II is a well-recognized stimulus for superoxide production through NADPH oxidase activation and opening of the mitochondrial ATP-sensitive potassium channels (mKATP). A role for this mechanism has been proposed to explain several physiological effects of the peptide. The aim of this study was to evaluate the involvement of this mechanism in the inotropic response to 100 nmol/L angiotensin II. Methods: Sarcomere shortening and intracellular pH (BCECF-epifluorescence technique) were evaluated in isolated cat ventricular myocytes placed in a perfusion chamber on the stage of an inverted microscope. Myocardial superoxide production was evaluated by the lucigenin quimioluminiscence method. Results: Angiotensin II (100 nmol/L) increased~70% sarcomere shortening, effect that was only partially prevented by NADPH oxidase inhibition,mKATP channel blockade or inhibition of the cardiac Na+/H+ exchanger (NHE-1). Moreover, angiotensin II stimulates NHE-1 activity by a NADPH oxidase-dependent mechanism. Myocardial superoxide production was also increased by angiotensin II, and this action was completely prevented either by NADPH oxidase inhibition or mKATP channel blockade. Conclusions: The positive inotropic response to 100 nmol/L angiotensin II is due to both ROS/NHE-1 dependent and independent pathways, this being a point of divergence with the signaling previously described to be triggered by lower concentrations of angiotensin II (i.e.: 1 nmol/L). |
publishDate |
2015 |
dc.date.none.fl_str_mv |
2015 |
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/10915/114769 |
url |
http://sedici.unlp.edu.ar/handle/10915/114769 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
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info:eu-repo/semantics/altIdentifier/issn/1054-8807 info:eu-repo/semantics/altIdentifier/doi/10.1016/j.carpath.2015.01.002 |
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info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/4.0/ Creative Commons Attribution 4.0 International (CC BY 4.0) |
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openAccess |
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http://creativecommons.org/licenses/by/4.0/ Creative Commons Attribution 4.0 International (CC BY 4.0) |
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application/pdf 236-240 |
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