A single resistance exercise session improved ACh-induced relaxation in the aortic rings of hypertensive rats compared to controls (Emax -80% vs -50%, p<0.05).
Does a single resistance exercise session improve aortic endothelial function in spontaneously hypertensive rats?
A single session of resistance exercise acutely improves aortic endothelial function in hypertensive rats, likely mediated by increased NO production via eNOS activation.
Absolute Event Rate: -80% vs -50%
p-value: p=<0.05
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 NG-nitro-L-arginine methyl ester (L-NAME) and indomethacin administration. The maximal response (Emax) and the sensitivity (EC50) to these drugs were evaluated. RESULTS: ACh-induced relaxation increased in the aortic rings of exercised (Ex) rats (Emax= -80 ± 4.6%, p < 0.05) when compared to those of controls (Ct) (Emax = -50 ± 6.8%). The Emax 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 (EC50= Ex -5.9 ± 0.14 vs. Ct -6.6 ± 0.33 log µM, p < 0.05 / Emax = 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.
Faria et al. (Sun,) conducted a other in Hypertension. Acute dynamic resistance exercise vs. Control (no exercise) was evaluated on ACh-induced relaxation (Emax) (p=<0.05). A single resistance exercise session improved ACh-induced relaxation in the aortic rings of hypertensive rats compared to controls (Emax -80% vs -50%, p<0.05).