Adjustments in β-adrenergic signaling contribute to the amelioration of cardiac dysfunction by exercise training in supravalvular aortic stenosis

Detalhes bibliográficos
Autor(a) principal: De Souza, Sérgio Luiz Borges [UNESP]
Data de Publicação: 2020
Outros Autores: Mota, Gustavo Augusto Ferreira [UNESP], Da Silvaa Paula Grippa Sant'Ana, Vitor Loureiro [UNESP], Vileigas, Danielle Fernandes [UNESP], De Campos, Dijon Henrique Salomé [UNESP], Padovani, Carlos Roberto [UNESP], Rodrigues, Maria Aparecida Marchesan [UNESP], Do Nascimento, André Ferreira, Sugizaki, Mario Mateus, Bazan, Silmeia Garcia Zanati [UNESP], Brum, Patrícia Chakur, Cicogna, Antonio Carlos [UNESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.33594/000000247
http://hdl.handle.net/11449/200722
Resumo: Background/Aims: Aortic stenosis-induced chronic pressure overload leads to cardiac dysfunction and congestive heart failure. The pathophysiological mechanisms of the myocardial impairment are multifactorial and include maladaptive β-adrenergic signaling. Exercise training (ET) has been used as a non-pharmacological therapy for heart failure management. The present study tested the hypothesis that exercise training attenuates diastolic dysfunction through β-adrenergic signaling preservation. Methods: Wistar rats were submitted to ascending aortic stenosis (AS) surgery, and after 18 weeks, a moderate aerobic exercise training protocol was performed for ten weeks. Results: ET attenuated diastolic dysfunction, evaluated by echocardiogram and isolated papillary muscle (IPM) assay. Also, ET reduced features of heart failure, cross-sectional cardiomyocyte area, and exercise intolerance, assessed by treadmill exercise testing. The β2 adrenergic receptor protein expression was increased in AS rats independently of exercise. Interestingly, ET restored the protein levels of phosphorylated phospholamban at Serine 16 and preserved the β-adrenergic receptor responsiveness as visualized by the lower myocardial compliance decline and time to 50% tension development and relaxation during β-adrenergic stimulation in the IPM than untrained rats. Additionally, AS rats presented higher levels of TNFα and iNOS, which were attenuated by ET. Conclusion: Moderate ET improves exercise tolerance, reduces heart failure features, and attenuates diastolic dysfunction. In the myocardium, ET decreases the cross-sectional area of the cardiomyocyte and preserves the β-adrenergic responsiveness, which reveals that the adjustments in β-adrenergic signaling contribute to the amelioration of cardiac dysfunction by mild exercise training in aortic stenosis rats.
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spelling Adjustments in β-adrenergic signaling contribute to the amelioration of cardiac dysfunction by exercise training in supravalvular aortic stenosisAortic bandageHeart failurePapillary musclePhysical trainingPressure overloadβ-adrenergic pathwayBackground/Aims: Aortic stenosis-induced chronic pressure overload leads to cardiac dysfunction and congestive heart failure. The pathophysiological mechanisms of the myocardial impairment are multifactorial and include maladaptive β-adrenergic signaling. Exercise training (ET) has been used as a non-pharmacological therapy for heart failure management. The present study tested the hypothesis that exercise training attenuates diastolic dysfunction through β-adrenergic signaling preservation. Methods: Wistar rats were submitted to ascending aortic stenosis (AS) surgery, and after 18 weeks, a moderate aerobic exercise training protocol was performed for ten weeks. Results: ET attenuated diastolic dysfunction, evaluated by echocardiogram and isolated papillary muscle (IPM) assay. Also, ET reduced features of heart failure, cross-sectional cardiomyocyte area, and exercise intolerance, assessed by treadmill exercise testing. The β2 adrenergic receptor protein expression was increased in AS rats independently of exercise. Interestingly, ET restored the protein levels of phosphorylated phospholamban at Serine 16 and preserved the β-adrenergic receptor responsiveness as visualized by the lower myocardial compliance decline and time to 50% tension development and relaxation during β-adrenergic stimulation in the IPM than untrained rats. Additionally, AS rats presented higher levels of TNFα and iNOS, which were attenuated by ET. Conclusion: Moderate ET improves exercise tolerance, reduces heart failure features, and attenuates diastolic dysfunction. In the myocardium, ET decreases the cross-sectional area of the cardiomyocyte and preserves the β-adrenergic responsiveness, which reveals that the adjustments in β-adrenergic signaling contribute to the amelioration of cardiac dysfunction by mild exercise training in aortic stenosis rats.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Department of Internal Medicine Botucatu Medical School São Paulo State UniversityDepartment of Biostatistics Institute of Biosciences of Botucatu São Paulo State UniversityDepartment of Pathology Botucatu Medical School São Paulo State UniversityInstitute of Health Science Federal University of Mato GrossoSchool of Physical Education and Sport University of São PauloDepartment of Internal Medicine Botucatu Medical School São Paulo State University (UNESP)Department of Internal Medicine Botucatu Medical School São Paulo State UniversityDepartment of Biostatistics Institute of Biosciences of Botucatu São Paulo State UniversityDepartment of Pathology Botucatu Medical School São Paulo State UniversityDepartment of Internal Medicine Botucatu Medical School São Paulo State University (UNESP)CAPES: 305399/2015-2CAPES: 442822/2014-6Universidade Estadual Paulista (Unesp)Federal University of Mato GrossoUniversidade de São Paulo (USP)De Souza, Sérgio Luiz Borges [UNESP]Mota, Gustavo Augusto Ferreira [UNESP]Da Silvaa Paula Grippa Sant'Ana, Vitor Loureiro [UNESP]Vileigas, Danielle Fernandes [UNESP]De Campos, Dijon Henrique Salomé [UNESP]Padovani, Carlos Roberto [UNESP]Rodrigues, Maria Aparecida Marchesan [UNESP]Do Nascimento, André FerreiraSugizaki, Mario MateusBazan, Silmeia Garcia Zanati [UNESP]Brum, Patrícia ChakurCicogna, Antonio Carlos [UNESP]2020-12-12T02:14:17Z2020-12-12T02:14:17Z2020-01-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article665-681http://dx.doi.org/10.33594/000000247Cellular Physiology and Biochemistry, v. 54, n. 4, p. 665-681, 2020.1421-97781015-8987http://hdl.handle.net/11449/20072210.33594/0000002472-s2.0-85087681930Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengCellular Physiology and Biochemistryinfo:eu-repo/semantics/openAccess2024-09-03T13:15:16Zoai:repositorio.unesp.br:11449/200722Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestrepositoriounesp@unesp.bropendoar:29462024-09-03T13:15:16Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Adjustments in β-adrenergic signaling contribute to the amelioration of cardiac dysfunction by exercise training in supravalvular aortic stenosis
title Adjustments in β-adrenergic signaling contribute to the amelioration of cardiac dysfunction by exercise training in supravalvular aortic stenosis
spellingShingle Adjustments in β-adrenergic signaling contribute to the amelioration of cardiac dysfunction by exercise training in supravalvular aortic stenosis
De Souza, Sérgio Luiz Borges [UNESP]
Aortic bandage
Heart failure
Papillary muscle
Physical training
Pressure overload
β-adrenergic pathway
title_short Adjustments in β-adrenergic signaling contribute to the amelioration of cardiac dysfunction by exercise training in supravalvular aortic stenosis
title_full Adjustments in β-adrenergic signaling contribute to the amelioration of cardiac dysfunction by exercise training in supravalvular aortic stenosis
title_fullStr Adjustments in β-adrenergic signaling contribute to the amelioration of cardiac dysfunction by exercise training in supravalvular aortic stenosis
title_full_unstemmed Adjustments in β-adrenergic signaling contribute to the amelioration of cardiac dysfunction by exercise training in supravalvular aortic stenosis
title_sort Adjustments in β-adrenergic signaling contribute to the amelioration of cardiac dysfunction by exercise training in supravalvular aortic stenosis
author De Souza, Sérgio Luiz Borges [UNESP]
author_facet De Souza, Sérgio Luiz Borges [UNESP]
Mota, Gustavo Augusto Ferreira [UNESP]
Da Silvaa Paula Grippa Sant'Ana, Vitor Loureiro [UNESP]
Vileigas, Danielle Fernandes [UNESP]
De Campos, Dijon Henrique Salomé [UNESP]
Padovani, Carlos Roberto [UNESP]
Rodrigues, Maria Aparecida Marchesan [UNESP]
Do Nascimento, André Ferreira
Sugizaki, Mario Mateus
Bazan, Silmeia Garcia Zanati [UNESP]
Brum, Patrícia Chakur
Cicogna, Antonio Carlos [UNESP]
author_role author
author2 Mota, Gustavo Augusto Ferreira [UNESP]
Da Silvaa Paula Grippa Sant'Ana, Vitor Loureiro [UNESP]
Vileigas, Danielle Fernandes [UNESP]
De Campos, Dijon Henrique Salomé [UNESP]
Padovani, Carlos Roberto [UNESP]
Rodrigues, Maria Aparecida Marchesan [UNESP]
Do Nascimento, André Ferreira
Sugizaki, Mario Mateus
Bazan, Silmeia Garcia Zanati [UNESP]
Brum, Patrícia Chakur
Cicogna, Antonio Carlos [UNESP]
author2_role author
author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade Estadual Paulista (Unesp)
Federal University of Mato Grosso
Universidade de São Paulo (USP)
dc.contributor.author.fl_str_mv De Souza, Sérgio Luiz Borges [UNESP]
Mota, Gustavo Augusto Ferreira [UNESP]
Da Silvaa Paula Grippa Sant'Ana, Vitor Loureiro [UNESP]
Vileigas, Danielle Fernandes [UNESP]
De Campos, Dijon Henrique Salomé [UNESP]
Padovani, Carlos Roberto [UNESP]
Rodrigues, Maria Aparecida Marchesan [UNESP]
Do Nascimento, André Ferreira
Sugizaki, Mario Mateus
Bazan, Silmeia Garcia Zanati [UNESP]
Brum, Patrícia Chakur
Cicogna, Antonio Carlos [UNESP]
dc.subject.por.fl_str_mv Aortic bandage
Heart failure
Papillary muscle
Physical training
Pressure overload
β-adrenergic pathway
topic Aortic bandage
Heart failure
Papillary muscle
Physical training
Pressure overload
β-adrenergic pathway
description Background/Aims: Aortic stenosis-induced chronic pressure overload leads to cardiac dysfunction and congestive heart failure. The pathophysiological mechanisms of the myocardial impairment are multifactorial and include maladaptive β-adrenergic signaling. Exercise training (ET) has been used as a non-pharmacological therapy for heart failure management. The present study tested the hypothesis that exercise training attenuates diastolic dysfunction through β-adrenergic signaling preservation. Methods: Wistar rats were submitted to ascending aortic stenosis (AS) surgery, and after 18 weeks, a moderate aerobic exercise training protocol was performed for ten weeks. Results: ET attenuated diastolic dysfunction, evaluated by echocardiogram and isolated papillary muscle (IPM) assay. Also, ET reduced features of heart failure, cross-sectional cardiomyocyte area, and exercise intolerance, assessed by treadmill exercise testing. The β2 adrenergic receptor protein expression was increased in AS rats independently of exercise. Interestingly, ET restored the protein levels of phosphorylated phospholamban at Serine 16 and preserved the β-adrenergic receptor responsiveness as visualized by the lower myocardial compliance decline and time to 50% tension development and relaxation during β-adrenergic stimulation in the IPM than untrained rats. Additionally, AS rats presented higher levels of TNFα and iNOS, which were attenuated by ET. Conclusion: Moderate ET improves exercise tolerance, reduces heart failure features, and attenuates diastolic dysfunction. In the myocardium, ET decreases the cross-sectional area of the cardiomyocyte and preserves the β-adrenergic responsiveness, which reveals that the adjustments in β-adrenergic signaling contribute to the amelioration of cardiac dysfunction by mild exercise training in aortic stenosis rats.
publishDate 2020
dc.date.none.fl_str_mv 2020-12-12T02:14:17Z
2020-12-12T02:14:17Z
2020-01-01
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.33594/000000247
Cellular Physiology and Biochemistry, v. 54, n. 4, p. 665-681, 2020.
1421-9778
1015-8987
http://hdl.handle.net/11449/200722
10.33594/000000247
2-s2.0-85087681930
url http://dx.doi.org/10.33594/000000247
http://hdl.handle.net/11449/200722
identifier_str_mv Cellular Physiology and Biochemistry, v. 54, n. 4, p. 665-681, 2020.
1421-9778
1015-8987
10.33594/000000247
2-s2.0-85087681930
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Cellular Physiology and Biochemistry
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 665-681
dc.source.none.fl_str_mv Scopus
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
repository.mail.fl_str_mv repositoriounesp@unesp.br
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