Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos
Autor(a) principal: | |
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Data de Publicação: | 2012 |
Outros Autores: | , , , , , |
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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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 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
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) |
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 |
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1808128104569241600 |