Adjustments in β-adrenergic signaling contribute to the amelioration of cardiac dysfunction by exercise training in supravalvular aortic stenosis
Autor(a) principal: | |
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Data de Publicação: | 2020 |
Outros Autores: | , , , , , , , , , , |
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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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 |
_version_ |
1810021390009499648 |