Effect of exercise on angiotensin (1-7) mediated vasodilation responses of aorta segments in nitric oxide synthase inhibition hypertension model

Objective: Although Renin-Angiotensin System (RAS) is involved in the pathogenesis of hypertension, its effects turn into protective with regular exercise. It has been revealed that newly identified RAS member Angiotensin (1-7) [Ang (1-7)] has antihypertensive effects. In our study, we aimed to investigate the affects of regular exercise on Ang (1-7)-mediated relaxation responses in hypertension. Method: 8-week-old male Wistar rats were divided into four groups as Control (C), Exercise (E), Hypertension (H) and Hypertension+Exercise (HE) groups. Hypertension was induced by nitric oxide synthase inhibitör administration to drinking water (25 mg.kg-1.day-1, 6 weeks). Swimming exercise was applied to the exercise groups for 6 weeks. The organ bath system was used to examine Ang (1-7)-mediated relaxation responses of the thoracic aorta. Contribution of endothelium-derived factors [NOS, cyclooxygenase (COX) and endothelium-derived hyperpolarizing factor (EDHF)], receptor antagonists of Mas [A-779 and D-Pro⁷-Ang(1-7)] and Angiotensin II Type 2 (AT2) receptor (PD123,319) were examined. Results: While blood pressure of the H group significantly increased compared to the C group; exercise treatment caused decreament in the HE group. Ang (1-7)-mediated relaxation responses was inreased in E and H groups compared to C. While Ang (1-7) mediated relaxation responses found to be decreased in all groups with NOS and EDHF inhibition; COX inhibition had no effect. While relaxation responses decreased only with D-Pro⁷-Ang(1-7) application in the K group, this effect was onserved with both Mas receptor antagonists in the E and HE groups. In group H, Ang (1-7) mediated relaxation responses were decreased in the presence of D-Pro⁷-Ang(1-7) and PD123,319 antagonists. Conclusion: We showed that the effect of exercise on Ang (1-7)-mediated relaxation responses in conductive vessels is mediated by the Mas receptor via NOS and EDHF pathways in the NOS inhibition hypertension model. Key words: NOS inhibition, hypertension, exercise, Ang (1-7)