Aerobic Exercise Training Prevents the Onset of Endothelial Dysfunction via Increased Nitric Oxide Bioavailability and Reduced Reactive Oxygen Species in an Experimental Model of Menopause
Autor(a) principal: | |
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Data de Publicação: | 2015 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://dx.doi.org/10.1371/journal.pone.0125388 http://repositorio.unifesp.br/handle/11600/39015 |
Resumo: | ObjectivePrevious studies have shown that estrogen deficiency, arising in postmenopause, promotes endothelial dysfunction. This study evaluated the effects of aerobic exercise training on endothelial dependent vasodilation of aorta in ovariectomized rats, specifically investigating the role of nitric oxide (NO) and reactive oxygen species (ROS).MethodsFemale Wistar rats ovariectomized (OVX - n= 20) or with intact ovary (SHAM - n= 20) remained sedentary (OVX and SHAM) or performed aerobic exercise training on a treadmill 5 times a week for a period of 8 weeks (OVX-TRA and SHAM-TRA). in the thoracic aorta the endothelium-dependent and - independent vasodilation was assessed by acetylcholine (ACh) and sodium nitroprusside (SNP), respectively. Certain aortic rings were incubated with L-NAME to assess the NO modulation on the ACh-induced vasodilation. the fluorescence to dihydroethidium in aortic slices and plasma nitrite/nitrate concentrations were measured to evaluate ROS and NO bioavailability, respectively.ResultsACh-induced vasodilation was reduced in OVX rats as compared SHAM (Rmax: SHAM: 86 +/-3.3 vs. OVX: 57+/-3.0%, p<0.01). Training prevented this response in OVX-TRA (Rmax: OVX-TRA: 88+/-2.0%, p<0.01), while did not change it in SHAM-TRA (Rmax: SHAM-TRA: 80+/-2.2%, p<0.01). the L-NAME incubation abolished the differences in ACh-induced relaxation among groups. SNP-induced vasodilation was not different among groups. OVX reduced nitrite/nitrate plasma concentrations and increased ROS in aortic slices, training as effective to restore these parameters to the SHAM levels.ConclusionsExercise training, even in estrogen deficiency conditions, is able to improve endothelial dependent vasodilation in rat aorta via enhanced NO bioavailability and reduced ROS levels. |
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Aerobic Exercise Training Prevents the Onset of Endothelial Dysfunction via Increased Nitric Oxide Bioavailability and Reduced Reactive Oxygen Species in an Experimental Model of MenopauseObjectivePrevious studies have shown that estrogen deficiency, arising in postmenopause, promotes endothelial dysfunction. This study evaluated the effects of aerobic exercise training on endothelial dependent vasodilation of aorta in ovariectomized rats, specifically investigating the role of nitric oxide (NO) and reactive oxygen species (ROS).MethodsFemale Wistar rats ovariectomized (OVX - n= 20) or with intact ovary (SHAM - n= 20) remained sedentary (OVX and SHAM) or performed aerobic exercise training on a treadmill 5 times a week for a period of 8 weeks (OVX-TRA and SHAM-TRA). in the thoracic aorta the endothelium-dependent and - independent vasodilation was assessed by acetylcholine (ACh) and sodium nitroprusside (SNP), respectively. Certain aortic rings were incubated with L-NAME to assess the NO modulation on the ACh-induced vasodilation. the fluorescence to dihydroethidium in aortic slices and plasma nitrite/nitrate concentrations were measured to evaluate ROS and NO bioavailability, respectively.ResultsACh-induced vasodilation was reduced in OVX rats as compared SHAM (Rmax: SHAM: 86 +/-3.3 vs. OVX: 57+/-3.0%, p<0.01). Training prevented this response in OVX-TRA (Rmax: OVX-TRA: 88+/-2.0%, p<0.01), while did not change it in SHAM-TRA (Rmax: SHAM-TRA: 80+/-2.2%, p<0.01). the L-NAME incubation abolished the differences in ACh-induced relaxation among groups. SNP-induced vasodilation was not different among groups. OVX reduced nitrite/nitrate plasma concentrations and increased ROS in aortic slices, training as effective to restore these parameters to the SHAM levels.ConclusionsExercise training, even in estrogen deficiency conditions, is able to improve endothelial dependent vasodilation in rat aorta via enhanced NO bioavailability and reduced ROS levels.Universidade Federal de São Paulo, Dept Biosci, São Paulo, BrazilUniv São Paulo, Inst Biomed Sci, Dept Physiol & Biophys, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biosci, São Paulo, BrazilWeb of ScienceFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)FAPESP: 2012/17709-0FAPESP: 2010/50048-1Public Library ScienceUniversidade Federal de São Paulo (UNIFESP)Universidade de São Paulo (USP)Braga, Viviane Aparecida Vieira Nogueira [UNIFESP]Couto, Gisele KrugerLazzarin, Mariana Cruz [UNIFESP]Rossoni, Luciana VenturiniMedeiros, Alessandra [UNIFESP]2016-01-24T14:40:25Z2016-01-24T14:40:25Z2015-04-29info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion13application/pdfhttp://dx.doi.org/10.1371/journal.pone.0125388Plos One. San Francisco: Public Library Science, v. 10, n. 4, 13 p., 2015.10.1371/journal.pone.0125388WOS000353711600146.pdf1932-6203http://repositorio.unifesp.br/handle/11600/39015WOS:000353711600146engPlos Oneinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-08-01T07:57:17Zoai:repositorio.unifesp.br/:11600/39015Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-08-01T07:57:17Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.none.fl_str_mv |
Aerobic Exercise Training Prevents the Onset of Endothelial Dysfunction via Increased Nitric Oxide Bioavailability and Reduced Reactive Oxygen Species in an Experimental Model of Menopause |
title |
Aerobic Exercise Training Prevents the Onset of Endothelial Dysfunction via Increased Nitric Oxide Bioavailability and Reduced Reactive Oxygen Species in an Experimental Model of Menopause |
spellingShingle |
Aerobic Exercise Training Prevents the Onset of Endothelial Dysfunction via Increased Nitric Oxide Bioavailability and Reduced Reactive Oxygen Species in an Experimental Model of Menopause Braga, Viviane Aparecida Vieira Nogueira [UNIFESP] |
title_short |
Aerobic Exercise Training Prevents the Onset of Endothelial Dysfunction via Increased Nitric Oxide Bioavailability and Reduced Reactive Oxygen Species in an Experimental Model of Menopause |
title_full |
Aerobic Exercise Training Prevents the Onset of Endothelial Dysfunction via Increased Nitric Oxide Bioavailability and Reduced Reactive Oxygen Species in an Experimental Model of Menopause |
title_fullStr |
Aerobic Exercise Training Prevents the Onset of Endothelial Dysfunction via Increased Nitric Oxide Bioavailability and Reduced Reactive Oxygen Species in an Experimental Model of Menopause |
title_full_unstemmed |
Aerobic Exercise Training Prevents the Onset of Endothelial Dysfunction via Increased Nitric Oxide Bioavailability and Reduced Reactive Oxygen Species in an Experimental Model of Menopause |
title_sort |
Aerobic Exercise Training Prevents the Onset of Endothelial Dysfunction via Increased Nitric Oxide Bioavailability and Reduced Reactive Oxygen Species in an Experimental Model of Menopause |
author |
Braga, Viviane Aparecida Vieira Nogueira [UNIFESP] |
author_facet |
Braga, Viviane Aparecida Vieira Nogueira [UNIFESP] Couto, Gisele Kruger Lazzarin, Mariana Cruz [UNIFESP] Rossoni, Luciana Venturini Medeiros, Alessandra [UNIFESP] |
author_role |
author |
author2 |
Couto, Gisele Kruger Lazzarin, Mariana Cruz [UNIFESP] Rossoni, Luciana Venturini Medeiros, Alessandra [UNIFESP] |
author2_role |
author author author author |
dc.contributor.none.fl_str_mv |
Universidade Federal de São Paulo (UNIFESP) Universidade de São Paulo (USP) |
dc.contributor.author.fl_str_mv |
Braga, Viviane Aparecida Vieira Nogueira [UNIFESP] Couto, Gisele Kruger Lazzarin, Mariana Cruz [UNIFESP] Rossoni, Luciana Venturini Medeiros, Alessandra [UNIFESP] |
description |
ObjectivePrevious studies have shown that estrogen deficiency, arising in postmenopause, promotes endothelial dysfunction. This study evaluated the effects of aerobic exercise training on endothelial dependent vasodilation of aorta in ovariectomized rats, specifically investigating the role of nitric oxide (NO) and reactive oxygen species (ROS).MethodsFemale Wistar rats ovariectomized (OVX - n= 20) or with intact ovary (SHAM - n= 20) remained sedentary (OVX and SHAM) or performed aerobic exercise training on a treadmill 5 times a week for a period of 8 weeks (OVX-TRA and SHAM-TRA). in the thoracic aorta the endothelium-dependent and - independent vasodilation was assessed by acetylcholine (ACh) and sodium nitroprusside (SNP), respectively. Certain aortic rings were incubated with L-NAME to assess the NO modulation on the ACh-induced vasodilation. the fluorescence to dihydroethidium in aortic slices and plasma nitrite/nitrate concentrations were measured to evaluate ROS and NO bioavailability, respectively.ResultsACh-induced vasodilation was reduced in OVX rats as compared SHAM (Rmax: SHAM: 86 +/-3.3 vs. OVX: 57+/-3.0%, p<0.01). Training prevented this response in OVX-TRA (Rmax: OVX-TRA: 88+/-2.0%, p<0.01), while did not change it in SHAM-TRA (Rmax: SHAM-TRA: 80+/-2.2%, p<0.01). the L-NAME incubation abolished the differences in ACh-induced relaxation among groups. SNP-induced vasodilation was not different among groups. OVX reduced nitrite/nitrate plasma concentrations and increased ROS in aortic slices, training as effective to restore these parameters to the SHAM levels.ConclusionsExercise training, even in estrogen deficiency conditions, is able to improve endothelial dependent vasodilation in rat aorta via enhanced NO bioavailability and reduced ROS levels. |
publishDate |
2015 |
dc.date.none.fl_str_mv |
2015-04-29 2016-01-24T14:40:25Z 2016-01-24T14:40:25Z |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1371/journal.pone.0125388 Plos One. San Francisco: Public Library Science, v. 10, n. 4, 13 p., 2015. 10.1371/journal.pone.0125388 WOS000353711600146.pdf 1932-6203 http://repositorio.unifesp.br/handle/11600/39015 WOS:000353711600146 |
url |
http://dx.doi.org/10.1371/journal.pone.0125388 http://repositorio.unifesp.br/handle/11600/39015 |
identifier_str_mv |
Plos One. San Francisco: Public Library Science, v. 10, n. 4, 13 p., 2015. 10.1371/journal.pone.0125388 WOS000353711600146.pdf 1932-6203 WOS:000353711600146 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Plos One |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
13 application/pdf |
dc.publisher.none.fl_str_mv |
Public Library Science |
publisher.none.fl_str_mv |
Public Library Science |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
biblioteca.csp@unifesp.br |
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1814268394519658496 |