Effect of swimming exercise on angiotensin-(1–7)-mediated aortic dilation responses in the nitric oxide synthase inhibition-induced hypertensive rats

OpenAlex İngilizce

Purpose: Regular exercise exerts at least some of its effects on lowering high blood pressure by regulating vascular tone. Angiotensin-(1-7) [Ang-(1-7)], a member of the renin–angiotensin system (RAS), has antihypertensive and vasodilator effects. The aim of this study is to investigate whether the blood pressure-lowering effect of regular exercise is mediated by Ang-(1-7)-induced vasodilation in a nitric oxide synthase (NOS) inhibition-induced hypertension model. Materials and Methods: 8-week-old Wistar male rats were separated into four groups: Control (C), Hypertension (H), Exercise (E), and Hypertension+Exercise (HE). Rats were subjected to the NOS inhibitor, Nω-nitro-L-arginine methyl ester (L-NAME,25 mg.kg-1.day-1) in drinking water and swimming (1 hour/day, 5 days/week) to create hypertension and/or exercise models. Ang-(1-7)-induced dilation responses of aortas were examined in the presence/absence of NOS, cyclooxygenase (COX), and endothelium-derived hyperpolarizing factor (EDHF) inhibitors. To assess the roles of the Mas receptor (MasR) and the Angiotensin II-Type2 receptor (AT2R) in Ang-(1-7)-induced vasodilation, the MasR antagonists A-779 and D-Pro⁷-Ang-(1-7), and AT2R inhibitor PD123319 were used. Results: Swimming exercise improved Ang-(1-7)-mediated vasodilation responses in the E but not in the HE group. Inhibition of NOS and EDHF pathways diminished Ang-(1-7)-induced vasodilation responses in all groups. While vasodilator responses were attenuated only by D-Pro⁷-Ang-(1-7) in the C group, both MasR antagonists reduced these responses in the E and HE groups. In the H group, Ang-(1-7)-induced vasodilation was decreased in the presence of both D-Pro⁷-Ang-(1-7) and PD123319. Conclusion: Although swimming exercise did not significantly alter Ang-(1-7)-mediated vasodilatory responses in the NOS-inhibited hypertensive model, an enhanced involvement of MasR receptors was observed in the vasodilation responses of the exercise groups, particularly through NOS and EDHF pathways.