dc.contributorUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:51:15Z
dc.date.available2014-05-20T13:51:15Z
dc.date.created2014-05-20T13:51:15Z
dc.date.issued2012-01-01
dc.identifierCellular Physiology and Biochemistry. Basel: Karger, v. 30, n. 5, p. 1191-1201, 2012.
dc.identifier1015-8987
dc.identifierhttp://hdl.handle.net/11449/18293
dc.identifier10.1159/000343309
dc.identifierWOS:000312617200009
dc.identifierWOS000312617200009.pdf
dc.identifier4463138671998432
dc.identifier5016839015394547[12]
dc.identifier1213140801402647
dc.identifier7438704034471673
dc.identifier0000-0002-9831-8820
dc.identifier0000-0002-9831-8820[12]
dc.identifier0000-0002-5843-6232
dc.description.abstractBackground/Aims: Renin-angiotensin-aldosterone system blockade with a mineralocorticoid-receptor antagonist has not yet been studied in exposure to tobacco smoke (TS) models. Thus, this study investigated the role of spironolactone on cardiac remodeling induced by exposure to tobacco smoke. Methods: Male Wistar rats were divided into 4 groups: a control group (group C, n=11); a group with 2 months of cigarette smoke exposure (group TS-C, n=13); a group that received spironolactone 20 mg/kg of diet/day and no cigarette smoke exposure (group TS-S, n=13); and a group with 2 months of cigarette smoke exposure and spironolactone supplementation (group S, n=12). The rats were observed for a period of 60 days, during which morphological, biochemical and functional analyses were performed. Results: There was no difference in invasive mean arterial pressure among the groups. There were no interactions between tobacco smoke exposure and spironolactone in the morphological and functional analysis. However, in the echocardiographic analysis, the TS groups had left chamber enlargement, higher left ventricular mass index and higher isovolumetric relaxation time corrected by heart rate compared with the non-TS groups. In vitro left ventricular diastolic function also worsened in the IS groups and was not influenced by spironolactone. In addition, there were no differences in myocardial levels of IFN-gamma, TNF-alpha, IL-10, ICAM-1 and GLUT4 [TS: OR 0.52, 95%CI (-0.007; 0.11); Spironolactone: OR -0.01, 95%CI (-0.07;0.05)]. Conclusion: Our data do not support the participation of aldosterone in the ventricular remodeling process induced by exposed to cigarette smoke. Copyright (C) 2012 S. Karger AG, Basel
dc.languageeng
dc.publisherKarger
dc.relationCellular Physiology and Biochemistry
dc.relation5.500
dc.relation1,561
dc.rightsAcesso aberto
dc.sourceWeb of Science
dc.subjectGLUT4
dc.subjectInflammation
dc.subjectVentricular remodeling
dc.subjectCigarette smoke
dc.titleAldosterone is not Involved in the Ventricular Remodeling Process Induced by Tobacco Smoke Exposure
dc.typeArtículos de revistas


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