dos Santos, Priscila P. [UNESP]Nogueira, Bruna F. [UNESP]Rafacho, Bruna P. M. [UNESP]Gaiolla, Paula Schmidt Azevedo [UNESP]Polegato, Bertha Furlan [UNESP]Chiuso-Minicucci, Fernanda [UNESP]Bonomo, Camila [UNESP]Roscani, Meliza Goi [UNESP]Zorzella-Pezavento, Sofia F. G. [UNESP]Tanni, Suzana E. [UNESP]Pereira, Elenize J. [UNESP]Okoshi, Marina Politi [UNESP]Paiva, Sergio Alberto Rupp de [UNESP]Zornoff, Leonardo Antonio Mamede [UNESP]Minicucci, Marcos Ferreira [UNESP]2014-05-202014-05-202012-01-01Cellular Physiology and Biochemistry. Basel: Karger, v. 30, n. 5, p. 1191-1201, 2012.1015-8987http://hdl.handle.net/11449/18293Background/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, Basel1191-1201engGLUT4InflammationVentricular remodelingCigarette smokeArtigo10.1159/000343309WOS:000312617200009Acesso abertoWOS000312617200009.pdf44631386719984325016839015394547[12]121314080140264774387040344716730000-0002-9831-88200000-0002-9831-8820[12]0000-0002-5843-6232