Swimming training improves the vasodilator effect of angiotensin-(1-7) in the aorta of spontaneously hypertensive rat.

Introduction: endothelial dysfunction plays a critical role in the pathogenesis of hypertension. It is well established that physical training has beneficial effects on the cardiovascular system. We recently reported that angiotensin-(1-7) [Ang-(1-7)] concentration and the Mas receptor expression is increased in the left ventricle of trained spontaneous hypertensive rats (SHR). The vascular effects of Ang-(1-7) in trained animals remain so far unknown. In the present study we investigated the effects of physical training on the vasodilator effect of Ang-(1-7) in the aorta of SHR.

Methodology: normotensive Wistar rats and SHR were subjected to an 8-wk period of 5% overload of body weight swimming training. Changes in isometric tension were recorded on myograph. Western blot was used to investigate Ang-(1-7) receptors expression.

Results: in aortas from normotensive rats Ang-(1-7) and ACh induced a concentration-dependent vasodilator effect, which was not modified by the physical training. Vessels from SHR had an impaired vasodilator response to Ang-(1-7) and ACh. The swimming training strongly potentiated the vasodilator effect induced by Ang-(1-7) in SHR, but did not modify the effect of ACh. Interestingly, Mas receptor protein expression was substantially increased by physical training in SHR. In trained SHR, the vasodilator effect of Ang-(1-7) was abrogated by removal of the endothelium and by the selective Ang-(1-7) receptor antagonists A-779 and d-Pro(7)-Ang-(1-7). l-NAME decreased Ang-(1-7) vasodilator response and indomethacin abolished the remaining dilatory response.

Conclusion: physical training increased Mas receptors expression in SHR aortas, thereby improving the vasodilator effect of Ang-(1-7) through an endothelium-dependent mechanism involving nitric oxide and prostacyclin.