Chronic stress improves the myocardial function without altering l-type ca+2 channel activity in rats
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/11449/227030 |
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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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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1808129293503430656 |