Chronic stress improves the myocardial function without altering l-type ca+2 channel activity in rats

Detalhes bibliográficos
Autor(a) principal: Bruder-Nascimento, Thiago [UNESP]
Data de Publicação: 2012
Outros Autores: Campos, Dijon Henrique Salome [UNESP], Leopoldo, André Soares, Lima-Leopoldo, Ana Paula, Okoshi, Katashi [UNESP], Cordellini, Sandra [UNESP], Cicogna, Antônio 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/11449/227030
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.
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spelling Chronic stress improves the myocardial function without altering l-type ca+2 channel activity in ratsCardiovascular diseases/psychologyPapillary musclesPhysiological/complicationsPhysiological/physiopathologyRatsStressBackground: 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.Department de Pharmacology Institute of Bioscience São Paulo State University (UNESP), Botucatu, SPDepartment de Pharmacology Medical School of Ribeirão Preto University of São Paulo (USP), Ribeirão Preto, SPDepartment of Medicine Clinical Botucatu School of Medicine São Paulo State University (UNESP), Botucatu, SPDepartment of Sports Center of Physical Education and Sports UFES - Federal University of Espirito Santo, Vitória, ESDepartment de Pharmacology Institute of Bioscience São Paulo State University (UNESP), Botucatu, SPDepartment of Medicine Clinical Botucatu School of Medicine São Paulo State University (UNESP), Botucatu, SPUniversidade Estadual Paulista (UNESP)Universidade de São Paulo (USP)UFES - Federal University of Espirito SantoBruder-Nascimento, Thiago [UNESP]Campos, Dijon Henrique Salome [UNESP]Leopoldo, André SoaresLima-Leopoldo, Ana PaulaOkoshi, Katashi [UNESP]Cordellini, Sandra [UNESP]Cicogna, Antônio Carlos [UNESP]2022-04-29T06:01:22Z2022-04-29T06:01:22Z2012-10-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article907-914http://dx.doi.org/10.1590/S0066-782X2012005000082Arquivos Brasileiros de Cardiologia, v. 99, n. 4, p. 907-914, 2012.0066-782X1678-4170http://hdl.handle.net/11449/22703010.1590/S0066-782X20120050000822-s2.0-84869004709Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengArquivos Brasileiros de Cardiologiainfo:eu-repo/semantics/openAccess2022-04-29T06:01:22Zoai:repositorio.unesp.br:11449/227030Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T21:10:33.891319Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Chronic stress improves the myocardial function without altering l-type ca+2 channel activity in rats
title Chronic stress improves the myocardial function without altering l-type ca+2 channel activity in rats
spellingShingle Chronic stress improves the myocardial function without altering l-type ca+2 channel activity in rats
Bruder-Nascimento, Thiago [UNESP]
Cardiovascular diseases/psychology
Papillary muscles
Physiological/complications
Physiological/physiopathology
Rats
Stress
title_short Chronic stress improves the myocardial function without altering l-type ca+2 channel activity in rats
title_full Chronic stress improves the myocardial function without altering l-type ca+2 channel activity in rats
title_fullStr Chronic stress improves the myocardial function without altering l-type ca+2 channel activity in rats
title_full_unstemmed Chronic stress improves the myocardial function without altering l-type ca+2 channel activity in rats
title_sort Chronic stress improves the myocardial function without altering l-type ca+2 channel activity in rats
author Bruder-Nascimento, Thiago [UNESP]
author_facet Bruder-Nascimento, Thiago [UNESP]
Campos, Dijon Henrique Salome [UNESP]
Leopoldo, André Soares
Lima-Leopoldo, Ana Paula
Okoshi, Katashi [UNESP]
Cordellini, Sandra [UNESP]
Cicogna, Antônio Carlos [UNESP]
author_role author
author2 Campos, Dijon Henrique Salome [UNESP]
Leopoldo, André Soares
Lima-Leopoldo, Ana Paula
Okoshi, Katashi [UNESP]
Cordellini, Sandra [UNESP]
Cicogna, Antônio 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)
UFES - Federal University of Espirito Santo
dc.contributor.author.fl_str_mv Bruder-Nascimento, Thiago [UNESP]
Campos, Dijon Henrique Salome [UNESP]
Leopoldo, André Soares
Lima-Leopoldo, Ana Paula
Okoshi, Katashi [UNESP]
Cordellini, Sandra [UNESP]
Cicogna, Antônio Carlos [UNESP]
dc.subject.por.fl_str_mv Cardiovascular diseases/psychology
Papillary muscles
Physiological/complications
Physiological/physiopathology
Rats
Stress
topic Cardiovascular diseases/psychology
Papillary muscles
Physiological/complications
Physiological/physiopathology
Rats
Stress
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.
publishDate 2012
dc.date.none.fl_str_mv 2012-10-01
2022-04-29T06:01:22Z
2022-04-29T06:01:22Z
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, v. 99, n. 4, p. 907-914, 2012.
0066-782X
1678-4170
http://hdl.handle.net/11449/227030
10.1590/S0066-782X2012005000082
2-s2.0-84869004709
url http://dx.doi.org/10.1590/S0066-782X2012005000082
http://hdl.handle.net/11449/227030
identifier_str_mv Arquivos Brasileiros de Cardiologia, v. 99, n. 4, p. 907-914, 2012.
0066-782X
1678-4170
10.1590/S0066-782X2012005000082
2-s2.0-84869004709
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Arquivos Brasileiros de Cardiologia
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 907-914
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
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