Abstract 526: Angiogenesis and Kallikrein-kinin System Activation after Exercise Training in Rats with Sustained Adrenergic Hyperactivity
Several mechanisms are involved to exercise-related cardioprotection.
Purpose Kallikrein-kinin system may contribute to this effect inducing endothelial vascular growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) expression.
Methods In a model of β-adrenergic hyperactivity, male Wistar rats were assigned into four groups: sedentary non-treated (Con); sedentary isoproterenol-treated (Iso); exercised only (Ex); and exercised isoproterenol-treated (Iso+Ex). Left ventricles were processed for Real time PCR and Western blot analysis in order to quantify the expression of kinins and angiogenic molecules.
Results In Iso+Ex, a significant increase of tissue kallikrein gene and protein expression was observed (p<0.01). In the same group, an augmented eNOS (p<0.05), VEGF and VEGF receptor mRNA expression (p<0.01) was observed. The expression of angiogenic IL-1 and Il-8 were increased after exercise (p<0.01). Expression of integrin linked kinase (ILK), another angiogenesis promoter, also augmented after training (p<0.01).
Conclusion Our results represent the first demonstration that exercise increases the tissue kallikrein gene and protein expression in rat myocardium after β-adrenergic hyperactivity. Together with the observed augmented eNOS and VEGF and angiogenesis-related molecules mRNA expression, a feasibly pathway might be drawn to understand the kallikrein-kinin system protective role to avoid the abnormalities developed due excessive catecholaminergic activation as observed in cardiac failure. Our data suggest a strong evidence of beneficial exercise action, particularly related to angiogenesis, in response of myocardium towards β-adrenergic hyperactivity.
- © 2013 by American Heart Association, Inc.