Extension of these findings were published elsewhere, and revealed that the beneficial role of exercise was accomplished by significant improvement in myocardial performance. In this study, there was complete protection from myocardial hypertrophy and dysfunction in rats that received isoproterenol after exercise. Fibrosis, apoptosis, and capillary reduction induced by isoproterenol were also blunted in exercised rats. Previous findings have raised interest regarding the possible mechanisms mediating the cardioprotective actions of exercise on sympathetic hyperactivity. The prevention of fibrosis, pro-inflammatory cytokines, oxidative stress, and apoptosis is of particular interest. The present study provides novel information regarding this issue. We found that the kallikrein-kinin system was positively modulated in the myocardial of rats on a regular exercise regime. Thus, tissue kallikrein expression at transcriptional and translational levels was augmented. These findings are interesting considering that cytoprotective effects have been linked to kallikrein. It was shown that protection by tissue kallikrein in oxidative organ damage is attributed to inhibition of apoptosis, inflammation, hypertrophy, and fibrosis. Tissue kallikrein knockout mice showed thinning of the LV wall and reduced myocardial mass compared with wild-type mice. These structural abnormalities were accompanied by reduced cardiac function, which was observed under basal conditions or acute b-adrenergic stimulation. Our findings suggest that tissue kallikrein is possibly Rapamycin msds participating in prevention of deleterious cardiac effects evoked by sympathetic hyperactivity in exercised rats. Regarding tissue kallikrein expression, the protein analysis corroborates gene expression, indicating that tissue kallikrein is highly formed in the myocardium. We showed that isoproterenol increased kinin B1 receptor mRNA expression, but exercise was able to inhibit this event. Interestingly, B2 receptor mRNA modulation only occurred in the exercised animals. There are no data linking deleterious or protective roles of bradykinin receptors in the heart on sympathetic hyperactivity. Therefore, it is difficult to speculate whether exercise-induced cardioprotection may be mediated by the synchronized effect on kinin B1 and B2 receptors. However, studies indicate a distinct role of these receptors in cardiac remodeling. Treatment with kinin B1 receptor antagonist improved cardiac function after myocardial infarction, as evidenced by attenuation of elevated LV end diastolic pressure. On the other hand, it was shown that tissue kallikrein, through the kinin B2 receptor and NO formation, improves cardiac function, apoptosis, and inflammation, and limits LV remodeling after ischemic injury. Additionally, it was shown that B2 receptor knockout mice subjected to myocardial infarction had a greater cardiomyocyte cross-sectional area and more interstitial collagen compared with wild-type controls. Studies have suggested a possible angiogenesis therapy using tissue kallikrein based on the fact that human tissue kallikrein was shown to be protective.