A Single Resistance Exercise Session Improves Aortic Endothelial Function in Hypertensive Rats

BACKGROUND: Physical exercise is an important tool for the improvement of endothelial function. OBJECTIVE: To assess the effects of acute dynamic resistance exercise on the endothelial function of spontaneously hypertensive rats (SHR). METHODS: Ten minutes after exercise, the aorta was removed to evaluate the expression of endothelial nitric oxide synthase (eNOS), phosphorylated endothelial nitric oxide synthase (p-eNOS1177) and inducible nitric oxide synthase (iNOS) and to generate concentration-response curves to acetylcholine (ACh) and to phenylephrine (PHE). The PHE protocol was also performed with damaged endothelium and before and after N(G)-nitro-L-arginine methyl ester (L-NAME) and indomethacin administration. The maximal response (E(max)) and the sensitivity (EC(50)) to these drugs were evaluated. RESULTS: ACh-induced relaxation increased in the aortic rings of exercised (Ex) rats (E(max)= -80 ± 4.6%, p < 0.05) when compared to those of controls (Ct) (E(max) = -50 ± 6.8%). The E(max) to PHE was decreased following exercise conditions (95 ± 7.9%, p < 0.05) when compared to control conditions (120 ± 4.2%). This response was abolished after L-NAME administration or endothelial damage. In the presence of indomethacin, the aortic rings' reactivity to PHE was decreased in both groups (EC(50)= Ex -5.9 ± 0.14 vs. Ct -6.6 ± 0.33 log µM, p < 0.05 / E(max) = Ex 9.5 ± 2.9 vs. Ct 17 ± 6.2%, p < 0.05). Exercise did not alter the expression of eNOS and iNOS, but increased the level of p-eNOS. CONCLUSION: A single resistance exercise session improves endothelial function in hypertensive rats. This response seems to be mediated by increased NO production through eNOS activation.