Paroxetine Alters Cardiac Stress Markers in Rats with Aortic Regurgitation

Background: Aortic regurgitation (AR) is a valvulopathy causes volume overload heart leading left ventricle dilation eccentric hypertrophy. A common co-morbidity associated with cardiovascular disease is depression. We have previously shown that paroxetine, a selective serotonin re-uptake inhibitor widely prescribed as antidepressant, improves contractility by preserving fractional shortening (FS) of AR rat hearts.In failing hearts, decrease of ability of myocardium generate an effective shortness velocity is well correlated with shift of myosin isoform distribution from α β- MyHC expression. In order understand mechanism involved improvement of FS treatment, we verified expression of involved heart contractility hypertrophy.Methods Findings: Male Wistar rats were submitted to AR surgery, by retrograde puncture of aortic valves leaflets, or sham surgery. Morphofunctional variables of the hearts were analyzed by echocardiograms at weeks 4 after induction of AR.At week 8 animals were euthanized for tissue collection posterior analysis of gene expression by RTq-PCR. Paroxetine treatment for 4 weeks AR rats reduced the gene expression of β-MyHC its myomiRs (miR-208 and miR-499). BNP, a molecular biomarker of hypertrophy, also showed their gene expression reduction after paroxetine treatment.Conclusion: These results suggest that paroxetine treatment improves FS AR hearts through reductions in expression of several genes involved with cardiac contractility hypertrophy.