Exercise improves endothelial function: A local analysis of production of nitric oxide and reactive oxygen species

Tanaka, Leonardo Yuji; Bechara, Luiz R. G.; Santos, Adriana Marques dos; Jordão, Camila Paixão; Sousa, Luís Gustavo Oliveira de; Bartholomeu, Teresa; Ventura, Liliane; Laurindo, Francisco Rafael Martins; Ramires, P. R.

doi:10.1016/j.niox.2015.01.003

Cited by 38 publications

(38 citation statements)

References 37 publications

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“…These results were confirmed by another study showing that the exercise-induced improvement in vasorelaxation depends on NO 28.…”

Section: Discussionsupporting

confidence: 71%

“…Therefore, the impaired vasodilation may be partially associated with NO production by eNOS. The maximal vasorelaxation induced by ACh after incubation with L-NAME was approximately 50%, consistent with the broad inhibitory effect of L-NAME on eNOS 28,34,35. Although the mechanisms underlying the variability in L-NAME effects are unclear and not addressed here, we cannot exclude the possibility that the effect was caused by loss-of-tension after noradrenaline-induced precontraction.…”

Section: Discussionsupporting

confidence: 64%

“…Based on previous studies conducted by our group, DHE (fluorescence detection) is sensitive for evaluating the superoxide levels 28,40. Thus, the analyses of Nox4 and superoxide levels suggest the development of an increasingly pro-oxidant status in SHR that increases NO degradation.…”

Section: Discussionmentioning

confidence: 98%

“…However, eNOS activity might have been increased because eNOS activity has been shown to increase in response to acute and chronic aerobic exercise 28,42.…”

Section: Discussionmentioning

confidence: 99%

“…After a 25-min washout period with warmed Krebs-bicarbonate buffer (pH 7.4, 37°C), the endothelium-independent vasorelaxation response to cumulative doses of sodium nitroprusside, an exogenous NO donor (SNP: 10 –11 to 10 –4 M), was assessed. All rings were precontracted with a submaximal 10 -7 M dose of noradrenaline 28.…”

Section: Methodsmentioning

confidence: 99%

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Aerobic Swim Training Restores Aortic Endothelial Function by Decreasing Superoxide Levels in Spontaneously Hypertensive Rats

Jordão

Fernandes

Tanaka

et al. 2017

Clinics

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OBJECTIVE:We aimed to determine whether aerobic training decreases superoxide levels, increases nitric oxide levels, and improves endothelium-dependent vasodilation in the aortas of spontaneously hypertensive rats.METHODS:Spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) were distributed into 2 groups: sedentary (SHRsd and WKYsd, n=10 each) and swimming-trained (SHRtr, n=10 and WKYtr, n=10, respectively). The trained group participated in training sessions 5 days/week for 1 h/day with an additional work load of 4% of the animal’s body weight. After a 10-week sedentary or aerobic training period, the rats were euthanized. The thoracic aortas were removed to evaluate the vasodilator response to acetylcholine (10-10 to 10-4 M) with or without preincubation with L-NG-nitro-L-arginine methyl ester hydrochloride (L-NAME; 10-4 M) in vitro. The aortic tissue was also used to assess the levels of the endothelial nitric oxide synthase and nicotinamide adenine dinucleotide oxidase subunit isoforms 1 and 4 proteins, as well as the superoxide and nitrite contents. Blood pressure was measured using a computerized tail-cuff system.RESULTS:Aerobic training significantly increased the acetylcholine-induced maximum vasodilation observed in the SHRtr group compared with the SHRsd group (85.9±4.3 vs. 71.6±5.2%). Additionally, in the SHRtr group, superoxide levels were significantly decreased, nitric oxide bioavailability was improved, and the levels of the nicotinamide adenine dinucleotide oxidase subunit isoform 4 protein were decreased compared to the SHRsd group. Moreover, after training, the blood pressure of the SHRtr group decreased compared to the SHRsd group. Exercise training had no effect on the blood pressure of the WKYtr group.CONCLUSIONS:In SHR, aerobic swim training decreased vascular superoxide generation by nicotinamide adenine dinucleotide oxidase subunit isoform 4 and increased nitric oxide bioavailability, thereby improving endothelial function.

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“…These results were confirmed by another study showing that the exercise-induced improvement in vasorelaxation depends on NO 28.…”

Section: Discussionsupporting

confidence: 71%

Section: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 98%

“…However, eNOS activity might have been increased because eNOS activity has been shown to increase in response to acute and chronic aerobic exercise 28,42.…”

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 3 more Smart Citations

Aerobic Swim Training Restores Aortic Endothelial Function by Decreasing Superoxide Levels in Spontaneously Hypertensive Rats

Jordão

Fernandes

Tanaka

et al. 2017

Clinics

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NO Signaling in the Cardiovascular System and Exercise

Fernandes

Gomes-Gatto

Pereira

et al. 2017

Advances in Experimental Medicine and Biology

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Nitric oxide (NO) is a small molecule implicated in multiple signal transduction pathways thus contributing to the regulation of many cellular functions. The identification of NO synthase (NOS) isoforms and the subsequent characterization of the mechanisms of cell activation of the enzymes permitted the partial understanding of both the physiological and pathological processes. NO bioavailability plays an important role in the pathophysiology of cardiovascular disease and its reduction in endothelial cells is strictly associated to endothelial dysfunction which, in turn, correlates with cardiovascular mortality. Indeed, endothelial NO synthase (eNOS) has a key role in limiting cardiac dysfunction and remodeling in heart diseases, in part by decreasing myocyte hypertrophy. Conversely, exercise training is recommended to prevent and treat cardiovascular diseases-associated disorders at least by enhanced NO synthase activity and expression, and increased production of antioxidants, which prevents premature breakdown of NO. Exercise training may cause an improvement in endothelial function for both experimental animals and humans; Studies in both healthy subjects and patients with impaired NO-related vasorelaxation remarked exercise training ability to improve vascular structure and function and endothelial homeostasis. This chapter will briefly consider the importance of NO signaling in the maintenance of cardiovascular physiology, and discuss recent insights into the effect of exercise training on the signaling pathways that modulate NO synthesis and degradation in health and cardiovascular disease. In addition, we will highlight the molecular mechanisms via which microRNAs (miRs) target NO signaling in the cardiovascular system, and NO as a candidate molecule for development of new therapies.

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Intermittent versus constant aerobic exercise in middle-aged males: acute effects on arterial stiffness and factors influencing the changes

Peres

Mourot

Ménétrier³

et al. 2018

Eur J Appl Physiol

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Exercise improves endothelial function: A local analysis of production of nitric oxide and reactive oxygen species

Cited by 38 publications

References 37 publications

Aerobic Swim Training Restores Aortic Endothelial Function by Decreasing Superoxide Levels in Spontaneously Hypertensive Rats

Aerobic Swim Training Restores Aortic Endothelial Function by Decreasing Superoxide Levels in Spontaneously Hypertensive Rats

NO Signaling in the Cardiovascular System and Exercise

Intermittent versus constant aerobic exercise in middle-aged males: acute effects on arterial stiffness and factors influencing the changes

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