Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos

Detalhes bibliográficos
Autor(a) principal: Bruder-Nascimento, Thiago [UNESP]
Data de Publicação: 2012
Outros Autores: Salome Campos, Dijon Henrique [UNESP], Leopoldo, Andre Soares, Lima-Leopoldo, Ana Paula, Okoshi, Katashi [UNESP], Cordellini, Sandra [UNESP], Cicogna, Antonio Carlos [UNESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.1590/S0066-782X2012005000082
http://hdl.handle.net/11449/11397
Resumo: Background: Chronic stress is associated with cardiac remodeling; however the mechanisms have yet to be clarified.Objective: The purpose of this study was test the hypothesis that chronic stress promotes cardiac dysfunction associated to L-type calcium Ca2+ channel activity depression.Methods: Thirty-day-old male Wistar rats (70 - 100 g) were distributed into two groups: control (C) and chronic stress (St). The stress was consistently maintained at immobilization during 15 weeks, 5 times per week, 1h per day. The cardiac function was evaluated by left ventricular performance through echocardiography and by ventricular isolated papillary muscle. The myocardial papillary muscle activity was assessed at baseline conditions and with inotropic maneuvers such as: post-rest contraction and increases in extracellular Ca2+ concentration, in presence or absence of specific blockers L-type calcium channels.Results: The stress was characterized for adrenal glands hypertrophy, increase of systemic corticosterone level and arterial hypertension. The chronic stress provided left ventricular hypertrophy. The left ventricular and baseline myocardial function did not change with chronic stress. However, it improved the response of the papillary muscle in relation to positive inotropic stimulation. This function improvement was not associated with the L-type Ca2+ channel.Conclusion: Chronic stress produced cardiac hypertrophy; however, in the study of papillary muscle, the positive inotropic maneuvers potentiated cardiac function in stressed rats, without involvement of L-type Ca2+ channel. Thus, the responsible mechanisms remain unclear with respect to Ca2+ influx alterations. (Arq Bras Cardiol 2012;99(4):907-914)
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spelling Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratosChronic Stress Improves the Myocardial Function without Altering L-type Ca+2 Channel Activity in RatsStress, physiological / complicationsstress, physiological / physiopathologycardiovascular diseases / psychologyratspapillary musclesBackground: Chronic stress is associated with cardiac remodeling; however the mechanisms have yet to be clarified.Objective: The purpose of this study was test the hypothesis that chronic stress promotes cardiac dysfunction associated to L-type calcium Ca2+ channel activity depression.Methods: Thirty-day-old male Wistar rats (70 - 100 g) were distributed into two groups: control (C) and chronic stress (St). The stress was consistently maintained at immobilization during 15 weeks, 5 times per week, 1h per day. The cardiac function was evaluated by left ventricular performance through echocardiography and by ventricular isolated papillary muscle. The myocardial papillary muscle activity was assessed at baseline conditions and with inotropic maneuvers such as: post-rest contraction and increases in extracellular Ca2+ concentration, in presence or absence of specific blockers L-type calcium channels.Results: The stress was characterized for adrenal glands hypertrophy, increase of systemic corticosterone level and arterial hypertension. The chronic stress provided left ventricular hypertrophy. The left ventricular and baseline myocardial function did not change with chronic stress. However, it improved the response of the papillary muscle in relation to positive inotropic stimulation. This function improvement was not associated with the L-type Ca2+ channel.Conclusion: Chronic stress produced cardiac hypertrophy; however, in the study of papillary muscle, the positive inotropic maneuvers potentiated cardiac function in stressed rats, without involvement of L-type Ca2+ channel. Thus, the responsible mechanisms remain unclear with respect to Ca2+ influx alterations. (Arq Bras Cardiol 2012;99(4):907-914)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)São Paulo State Univ, UNESP, Inst Biosci, Dept Pharmacol, Botucatu, SP, BrazilUniv São Paulo, Dept Pharmacol, Med Sch Ribeirao Preto, BR-14049 Ribeirao Preto, SP, BrazilSão Paulo State Univ, UNESP, Dept Clin Med, Botucatu Sch Med, Botucatu, SP, BrazilUFES Fed Univ Espirito Santo, Ctr Phys Educ & Sports, Dept Sports, Vitoria, ES, BrazilSão Paulo State Univ, UNESP, Inst Biosci, Dept Pharmacol, Botucatu, SP, BrazilSão Paulo State Univ, UNESP, Dept Clin Med, Botucatu Sch Med, Botucatu, SP, BrazilFAPESP: 09/03771-2Arquivos Brasileiros CardiologiaUniversidade Estadual Paulista (Unesp)Universidade de São Paulo (USP)Universidade Federal do Espírito Santo (UFES)Bruder-Nascimento, Thiago [UNESP]Salome Campos, Dijon Henrique [UNESP]Leopoldo, Andre SoaresLima-Leopoldo, Ana PaulaOkoshi, Katashi [UNESP]Cordellini, Sandra [UNESP]Cicogna, Antonio Carlos [UNESP]2014-05-20T13:33:19Z2014-05-20T13:33:19Z2012-10-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article907-914application/pdfapplication/pdfhttp://dx.doi.org/10.1590/S0066-782X2012005000082Arquivos Brasileiros de Cardiologia. Rio de Janeiro: Arquivos Brasileiros Cardiologia, v. 99, n. 4, p. 907-914, 2012.0066-782Xhttp://hdl.handle.net/11449/11397S0066-782X2012001300006WOS:000310542300009S0066-782X2012001300006-pt.pdfS0066-782X2012001300006-en.pdf561648831769003794189701035641371590971576309420Web of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengArquivos Brasileiros de Cardiologia1.318info:eu-repo/semantics/openAccess2024-08-14T17:21:54Zoai:repositorio.unesp.br:11449/11397Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-14T17:21:54Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos
Chronic Stress Improves the Myocardial Function without Altering L-type Ca+2 Channel Activity in Rats
title Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos
spellingShingle Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos
Bruder-Nascimento, Thiago [UNESP]
Stress, physiological / complications
stress, physiological / physiopathology
cardiovascular diseases / psychology
rats
papillary muscles
title_short Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos
title_full Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos
title_fullStr Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos
title_full_unstemmed Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos
title_sort Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos
author Bruder-Nascimento, Thiago [UNESP]
author_facet Bruder-Nascimento, Thiago [UNESP]
Salome Campos, Dijon Henrique [UNESP]
Leopoldo, Andre Soares
Lima-Leopoldo, Ana Paula
Okoshi, Katashi [UNESP]
Cordellini, Sandra [UNESP]
Cicogna, Antonio Carlos [UNESP]
author_role author
author2 Salome Campos, Dijon Henrique [UNESP]
Leopoldo, Andre Soares
Lima-Leopoldo, Ana Paula
Okoshi, Katashi [UNESP]
Cordellini, Sandra [UNESP]
Cicogna, Antonio Carlos [UNESP]
author2_role author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade Estadual Paulista (Unesp)
Universidade de São Paulo (USP)
Universidade Federal do Espírito Santo (UFES)
dc.contributor.author.fl_str_mv Bruder-Nascimento, Thiago [UNESP]
Salome Campos, Dijon Henrique [UNESP]
Leopoldo, Andre Soares
Lima-Leopoldo, Ana Paula
Okoshi, Katashi [UNESP]
Cordellini, Sandra [UNESP]
Cicogna, Antonio Carlos [UNESP]
dc.subject.por.fl_str_mv Stress, physiological / complications
stress, physiological / physiopathology
cardiovascular diseases / psychology
rats
papillary muscles
topic Stress, physiological / complications
stress, physiological / physiopathology
cardiovascular diseases / psychology
rats
papillary muscles
description Background: Chronic stress is associated with cardiac remodeling; however the mechanisms have yet to be clarified.Objective: The purpose of this study was test the hypothesis that chronic stress promotes cardiac dysfunction associated to L-type calcium Ca2+ channel activity depression.Methods: Thirty-day-old male Wistar rats (70 - 100 g) were distributed into two groups: control (C) and chronic stress (St). The stress was consistently maintained at immobilization during 15 weeks, 5 times per week, 1h per day. The cardiac function was evaluated by left ventricular performance through echocardiography and by ventricular isolated papillary muscle. The myocardial papillary muscle activity was assessed at baseline conditions and with inotropic maneuvers such as: post-rest contraction and increases in extracellular Ca2+ concentration, in presence or absence of specific blockers L-type calcium channels.Results: The stress was characterized for adrenal glands hypertrophy, increase of systemic corticosterone level and arterial hypertension. The chronic stress provided left ventricular hypertrophy. The left ventricular and baseline myocardial function did not change with chronic stress. However, it improved the response of the papillary muscle in relation to positive inotropic stimulation. This function improvement was not associated with the L-type Ca2+ channel.Conclusion: Chronic stress produced cardiac hypertrophy; however, in the study of papillary muscle, the positive inotropic maneuvers potentiated cardiac function in stressed rats, without involvement of L-type Ca2+ channel. Thus, the responsible mechanisms remain unclear with respect to Ca2+ influx alterations. (Arq Bras Cardiol 2012;99(4):907-914)
publishDate 2012
dc.date.none.fl_str_mv 2012-10-01
2014-05-20T13:33:19Z
2014-05-20T13:33:19Z
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/10.1590/S0066-782X2012005000082
Arquivos Brasileiros de Cardiologia. Rio de Janeiro: Arquivos Brasileiros Cardiologia, v. 99, n. 4, p. 907-914, 2012.
0066-782X
http://hdl.handle.net/11449/11397
S0066-782X2012001300006
WOS:000310542300009
S0066-782X2012001300006-pt.pdf
S0066-782X2012001300006-en.pdf
5616488317690037
9418970103564137
1590971576309420
url http://dx.doi.org/10.1590/S0066-782X2012005000082
http://hdl.handle.net/11449/11397
identifier_str_mv Arquivos Brasileiros de Cardiologia. Rio de Janeiro: Arquivos Brasileiros Cardiologia, v. 99, n. 4, p. 907-914, 2012.
0066-782X
S0066-782X2012001300006
WOS:000310542300009
S0066-782X2012001300006-pt.pdf
S0066-782X2012001300006-en.pdf
5616488317690037
9418970103564137
1590971576309420
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Arquivos Brasileiros de Cardiologia
1.318
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eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 907-914
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Arquivos Brasileiros Cardiologia
publisher.none.fl_str_mv Arquivos Brasileiros Cardiologia
dc.source.none.fl_str_mv Web of Science
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
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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)
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