Chronic exercise enhances vascular responses to clonidine in rats by increasing endothelial alpha2-adrenergic...

Chronic exercise increases endothelium-dependent vasodilating responses. To investigate whether endothelial alpha2-adrenergic receptor upregulation is involved in the enhancement of clonidine-induced vasorelaxation by chronic exercise, 4-week-old male Wistar rats were used. They were divided into control and exercise groups. The trained animals ran on a treadmill at a moderate intensity for 60 min per day, 5 days per week for 10 weeks in total. Resting heart rates were measured by a tail-cuff method to confirm training effects. After training, rings of the thoracic aorta were prepared to evaluate vasodilating responses to clonidine, an alpha2 agonist. Released endothelium-derived relaxing factors were pharmacologically identified by treatment of N(omega)-nitro-L-arginine, a nitric oxide (NO) synthase inhibitor, or tetraethylammonium chloride, an endothelium-derived hyperpolarization factor (EDHF) inhibitor. Receptor binding assays were performed by using 3H-labeled clonidine as a tracer. We found that chronic exercise enhanced vascular responses to clonidine by stimulating the release of both NO and EDHF. It also increased the binding affinity of endothelial cell alpha2 receptor without changing the number of binding sites. Therefore, the elevated vasorelaxing responses to clonidine after chronic exercise may be partially resulted from an increase in endothelial alpha2 receptor binding affinity.