| Grant number: | 12/21019-9 |
| Support Opportunities: | Regular Research Grants - Publications - Scientific article |
| Start date: | December 01, 2012 |
| End date: | May 31, 2013 |
| Field of knowledge: | Biological Sciences - Physiology - Physiology of Organs and Systems |
| Principal Investigator: | Marcos Ferreira Minicucci |
| Grantee: | Marcos Ferreira Minicucci |
| Host Institution: | Faculdade de Medicina (FMB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil |
| City of the host institution: | Botucatu |
Abstract
Background/Aims: Renin-angiotensin-aldosterone system blockade with a mineralocorticoid-receptor antagonist has not yet been studied in exposure to tobacco smoke (ETS) models. Thus, this study investigated the role of spironolactone on cardiac remodeling induced by ETS.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 ETS-C, n=13); a group that received spironolactone 20 mg/kg of diet/day and no cigarette smoke exposure (group ETS-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 ETS groups had left chamber enlargement, higher left ventricular mass index and higher isovolumetric relaxation time corrected by heart rate compared with the non-ETS groups. In vitro left ventricular diastolic function also worsened in the ETS groups and was not influenced by spironolactone. In addition, there were no differences in myocardial levels of IFN-³, TNF-±, IL-10, ICAM-1 and GLUT4 [ETS: 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. (AU)
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