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

Abstract

BackgroundPhysical exercise is an important tool for the improvement of endothelial function.ObjectiveTo assess the effects of acute dynamic resistance exercise on the endothelial function of spontaneously hypertensive rats (SHR).MethodsTen 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.ConclusionA single resistance exercise session improves endothelial function in hypertensive rats. This response seems to be mediated by increased NO production through eNOS activation.

Impact of Lifestyles (Diet and Exercise) on Vascular Health: Oxidative Stress and Endothelial Function

“…It is also suggested that the stimulation of NO production is dependent on the volume of exercise, and a greater demand of oxygen and nutrients is involved in the beneficial effects of exercise on the endothelium [ 263 , 266 ]. Moreover, similar results are observed in hypertensive rats that single session of resisted exercise activates eNOS and promotes vasorelaxation [ 267 ]. Interestingly, expression of the prooxidant enzyme, NADPH oxidase, is reduced by exercise training in hypertensive rats, which may have a beneficial effect on the half-life of NO in the vascular wall [ 266 ].…”

Mulberry Extract Attenuates Endothelial Dysfunction through the Regulation of Uncoupling Endothelial Nitric Oxide Synthase in High Fat Diet Rats

“…Among the studied phosphorylation of eNOS sites, Thr495 and Serine 114, 615 and 633, the phosphorylation of Ser1177 or Thr495 is particularly important [38]. Although there has been debate about the role of Thr495 phosphorylation about NOS activity [22,23], the role of Ser1177 phosphorylation has been relatively well established as a positive post-translational modification for NOS activity [39]. Here, in the presence of mulberry, the phosphorylation of Thr495 and Ser1177 rather increased, enhancing NO release, consistent to a recent study of mulberry [11].…”

Effects of resistance exercise on endothelial progenitor cell mobilization in women

“…A recent systematic review and dose–response meta-analysis showed that resistance exercise training improves endothelial function and that greater frequency, rather than intensity, is the key factor to maximize improvement in flow-mediated dilation 34 ; per opposition to the chronic effects, the acute effects of resistance exercise on endothelial function are not consensual. Some evidence has shown that acute high-intensity resistance eccentric exercise 35 may decrease endothelial function, whereas dynamic submaximal resistance exercise seems to acutely improve endothelial function in hypertensive rats 36 , 37 , type 2 diabetes patients 38 and healthy males 39 .…”