Acute effect of brisk walking with graduated compression stockings on vascular endothelial function and oxidative stress

2013 ◽  
pp. n/a-n/a ◽  
Author(s):  
Takanobu Okamoto ◽  
Mikako Sakamaki-Sunaga ◽  
Seokki Min ◽  
Takashi Miura ◽  
Tetsuji Iwasaki
Keyword(s):  
Oxidative Stress ◽  
Endothelial Function ◽  
Acute Effect ◽  
Vascular Endothelial ◽  
Brisk Walking ◽  
Vascular Endothelial Function ◽  
Compression Stockings ◽  
Graduated Compression Stockings ◽  
And Oxidative Stress

scholarly journals Vascular endothelial function and oxidative stress are related to dietary niacin intake among healthy middle-aged and older adults

2014 ◽  
Vol 116 (2) ◽  
pp. 156-163 ◽  
Author(s):  
Rachelle E. Kaplon ◽  
Lindsey B. Gano ◽  
Douglas R. Seals
Keyword(s):  
Oxidative Stress ◽  
Older Adults ◽  
Nadph Oxidase ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Antioxidant Vitamin ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Middle Aged ◽  
And Oxidative Stress

We tested the hypothesis that vascular endothelial function and oxidative stress are related to dietary niacin intake among healthy middle-aged and older adults. In 127 men and women aged 48–77 yr, brachial artery flow-mediated dilation (FMD) was positively related to dietary niacin intake [%change (Δ): r = 0.20, P < 0.05; mmΔ: r = 0.25, P < 0.01]. In subjects with above-average dietary niacin intake (≥22 mg/day, NHANES III), FMD was 25% greater than in subjects with below-average intake ( P < 0.05). Stepwise linear regression revealed that dietary niacin intake (above vs. below average) was an independent predictor of FMD (%Δ: β = 1.8; mmΔ: β = 0.05, both P < 0.05). Plasma oxidized low-density lipoprotein, a marker of systemic oxidative stress, was inversely related to niacin intake ( r = −0.23, P < 0.05) and was lower in subjects with above- vs. below-average niacin intake (48 ± 2 vs. 57 ± 2 mg/dl, P < 0.01). Intravenous infusion of the antioxidant vitamin C improved brachial FMD in subjects with below-average niacin intake ( P < 0.001, n = 33), but not above-average ( P > 0.05, n = 20). In endothelial cells sampled from the brachial artery of a subgroup, dietary niacin intake was inversely related to nitrotyrosine, a marker of peroxynitrite-mediated oxidative damage ( r = −0.30, P < 0.05, n = 55), and expression of the prooxidant enzyme, NADPH oxidase ( r = −0.44, P < 0.01, n = 37), and these markers were lower in subjects with above- vs. below-average niacin intake [nitrotyrosine: 0.39 ± 0.05 vs. 0.56 ± 0.07; NADPH oxidase: 0.38 ± 0.05 vs. 0.53 ± 0.05 (ratio to human umbilical vein endothelial cell control), both P < 0.05]. Our findings support the hypothesis that higher dietary niacin intake is associated with greater vascular endothelial function related to lower systemic and vascular oxidative stress among healthy middle-aged and older adults.

scholarly journals SUMO2 regulates vascular endothelial function and oxidative stress in mice

2019 ◽  
Vol 317 (6) ◽  
pp. H1292-H1300 ◽  
Author(s):  
Young-Rae Kim ◽  
Julia S. Jacobs ◽  
Qiuxia Li ◽  
Ravinder Reddy Gaddam ◽  
Ajit Vikram ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Function ◽  
Vascular Function ◽  
Ex Vivo ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Density Lipoprotein Receptor ◽  
Vascular Oxidative Stress

SUMOylation is a posttranslational modification of lysine residues. Modification of proteins by small ubiquitin-like modifiers (SUMO)1, -2, and -3 can achieve varied, and often unique, physiological and pathological effects. We looked for SUMO2-specific effects on vascular endothelial function. SUMO2 expression was upregulated in the aortic endothelium of hypercholesterolemic low-density lipoprotein receptor-deficient mice and was responsible for impairment of endothelium-dependent vasorelaxation in these mice. Moreover, overexpression of SUMO2 in aortas ex vivo, in cultured endothelial cells, and transgenically in the endothelium of mice increased vascular oxidative stress and impaired endothelium-dependent vasorelaxation. Conversely, inhibition of SUMO2 impaired physiological endothelium-dependent vasorelaxation in normocholesterolemic mice. These findings indicate that while endogenous SUMO2 is important in maintenance of normal endothelium-dependent vascular function, its upregulation impairs vascular homeostasis and contributes to hypercholesterolemia-induced endothelial dysfunction. NEW & NOTEWORTHY Sumoylation is known to impair vascular function; however, the role of specific SUMOs in the regulation of vascular function is not known. Using multiple complementary approaches, we show that hyper-SUMO2ylation impairs vascular endothelial function and increases vascular oxidative stress, whereas endogenous SUMO2 is essential for maintenance of normal physiological function of the vascular endothelium.

P941Acute effects of electronic hookah smoking on endothelial function, inflammation and oxidative stress

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Rezk-Hanna ◽  
E Ricci ◽  
E Ikharo ◽  
M L Brecht
Keyword(s):  
Oxidative Stress ◽  
Mean Arterial Pressure ◽  
Vitamin C ◽  
Endothelial Function ◽  
Acute Effect ◽  
Plasma Nicotine ◽  
Tnf Α ◽  
Before And After ◽  
Hookah Smoking ◽  
And Oxidative Stress

Abstract Background Electronic nicotine delivery systems (ENDS) are a new rapidly growing global epidemic. More recently, electronic (e-) hookahs, have increased in popularity in the United States, with the greatest uptake by young female adults, who endorse marketing claims that these products are safer alternatives to traditional hookah tobacco smoking. Unlike other ENDS such as e-cigarettes, e-hookah bowls are used through traditional waterpipes, allowing the vapor–containing aerosolized nicotine, propylene glycol, glycerin, and flavorings–to pass through a water-filled basin, before it is inhaled through the user's mouth. Contributing to e-hookah bowls' popularity is the belief that e-hookah flavored smoke is detoxified as it passes through the water-filled basin, rendering e-hookah a safer tobacco alternative. However, an e-hookah bowl delivers flavored nicotine by creating a vapor of fine (<2.5 μm) and ultrafine particles (<0.1 μm) that could induce vascular toxicity. Purpose To test the acute effect of electronic hookah smoking on endothelial function, inflammation and oxidative stress. Methods In 17 healthy young adults who smoke hookah but not cigarettes (age 26±1 years, mean±SE; BMI 23.8±0.7 kg-m2), we measured brachial artery flow-mediated dilation (FMD) before and after a 30-minute e-hookah bowl smoking. To test for inflammatory mediation, pro-inflammatory cytokines hsCRP, TNF-α, and fibrinogen were collected before and after smoking. To test for oxidative stress mediation, on a separate day, the acute effect of e-hookah smoking on FMD was examined after intravenous infusion of Vitamin C, an effective antioxidant. Plasma nicotine levels were collected before and after the smoking session. The same measurements were performed before and after a subset of subjects (n=8) performed a sham-smoking control study. Results E-hookah smoking, which markedly increased plasma nicotine (Δ plasma nicotine: +6.07±1.87, p=0.018) and mean arterial pressure (Δ mean arterial pressure: +12±2 mm Hg, p<0.001), acutely decreased FMD from 8.04±0.68 to 6.14±0.52%Δ, p<0.001, indicating impaired endothelial function. While fibrinogen and TNF-α levels increased from 225.31±7.41 to 236.77±9.79, p=0.026 and from 0.80±0.04 to 0.87±0.05, p=0.036, respectively, hsCRP did not change (P=ns). Vitamin C administration prevented the acute FMD impairment by e-hookah smoking (P=ns). All parameters were unchanged during sham-control studies. Conclusions In contrast to the widespread popular belief that e-hookah is safe, the data herein show that each e-hookah session constitutes a potent vascular toxin acutely impairing endothelial function and inducing an inflammatory state. That the acute impairment in FMD with electronic hookah is restored with administration of the potent antioxidant Vitamin C suggest that elevated vascular oxidative stress as a key mechanism involved. These new data provide evidence to counter claims that e-hookah is a safer tobacco alternative. Acknowledgement/Funding This work was funded by the National Institutes of Health, National Heart, Lung, and Blood Institute 1R21HL145002-01 to MRH.

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