Improved arterial flow-mediated dilation after exertion involves hydrogen peroxide in overweight and obese adults following aerobic exercise training

Robinson, Austin T.; Franklin, Nina C.; Norkeviciute, Edita; Bian, Jing; Babana, James C.; Szczurek, Mary; Phillips, Shane A.

doi:10.1097/hjh.0000000000000946

Cited by 32 publications

(63 citation statements)

References 40 publications

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“…The mediator of FID in human adipose is typically NO under normal physiological conditions (Phillips et al., ). Consistent with the results of our previous studies (Phillips et al., ; Robinson et al., ), we found that NO is the primary mediator of dilation to flow in subcutaneous adipose RAs. Previous studies have found that, in the setting of CV disease or presence of CV risk factors such as hypertension, NO is scavenged by elevated levels of reactive oxygen species (Erdei et al., ; Guzik et al., ).…”

Section: Discussionsupporting

confidence: 93%

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MicroRNA‐21 Contributes to Reduced Microvascular Function in Binge Drinking Young Adults

Bian

Piano

Kotlo

et al. 2017

Alcoholism Clin & Exp Res

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Section: Discussionsupporting

confidence: 93%

“…As previously described, we used resistance arteries (RAs) in subcutaneous fat to investigate microvascular function in humans (Durand et al., ; Robinson et al., ). Approximately 2 ml of fat tissue was removed and transferred to (4°C) HEPES solution.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA‐21 Contributes to Reduced Microvascular Function in Binge Drinking Young Adults

Bian

Piano

Kotlo

et al. 2017

Alcoholism Clin & Exp Res

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“…Nitric oxide and ROS generation were measured simultaneously in isolated skeletal muscle arterioles as previously described [30] using Enzo Life Sciences NO Detection Kit and ROS indicator (2′,7′-dichlorodihydrofluorescein diacetate (H 2 DCFDA); ThermoFisher Scientific). Flow-induced nitric oxide and ROS production were measured in microvessels following cannulation and maintenance of 37 °C in a 20 ml aerated organ chambers, bathed in Krebs solution chamber at an equilibration pressure of 60 cm H 2 O for 60 min.…”

Section: Methodsmentioning

confidence: 99%

Nox2 contributes to hyperinsulinemia-induced redox imbalance and impaired vascular function

et al. 2017

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Insulin resistance promotes vascular endothelial dysfunction and subsequent development of cardiovascular disease. Previously we found that skeletal muscle arteriolar flow-induced dilation (FID) was reduced following a hyperinsulinemic clamp in healthy adults. Therefore, we hypothesized that hyperinsulinemia, a hallmark of insulin resistance, contributes to microvascular endothelial cell dysfunction via inducing oxidative stress that is mediated by NADPH oxidase (Nox) system. We examined the effect of insulin, at levels that are comparable with human hyperinsulinemia on 1) FID of isolated arterioles from human skeletal muscle tissue in the presence and absence of Nox inhibitors and 2) human adipose microvascular endothelial cell (HAMECs) expression of nitric oxide (NO), endothelial NO synthase (eNOS), and Nox-mediated oxidative stress. In six lean healthy participants (mean age 25.5±1.6 y, BMI 21.8±0.9), reactive oxygen species (ROS) were increased while NO and arteriolar FID were reduced following 60 min of ex vivo insulin incubation. These changes were reversed after co-incubation with the Nox isoform 2 (Nox2) inhibitor, VAS2870. In HAMECs, insulin-induced time-dependent increases in Nox2 expression and P47phox phosphorylation were echoed by elevations of superoxide production. In contrast, phosphorylation of eNOS and expression of superoxide dismutase (SOD2 and SOD3) isoforms showed a biphasic response with an increased expression at earlier time points followed by a steep reduction phase. Insulin induced eNOS uncoupling that was synchronized with a drop of NO and a surge of ROS production. These effects were reversed by Tempol (SOD mimetic), Tetrahydrobiopterin (BH4; eNOS cofactor), and VAS2870. Finally, insulin induced nitrotyrosine formation which was reversed by inhibiting NO or superoxide generation. In conclusions, hyperinsulinemia may reduce FID via inducing Nox2-mediated superoxide production in microvascular endothelial cells which reduce the availability of NO and enhances peroxynitrite formation. Therefore, the Nox2 pathway should be considered as a target for the prevention of oxidative stress-associated endothelial dysfunction during hyperinsulinemia.

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“…Experimental findings demonstrate that exercise training is able to prevent and improve endothelial dysfunction. Furthermore, management of CV risk factors also tends to improve or restore endothelial function [9,50] .…”

Section: Exercise Arterial Function and Cardiac Rehabilitationmentioning

confidence: 99%

“…Since acute stress to the vascular endothelium is linked to higher incidence of CVD, physical exercise practice appears to be fundamental to protect against vascular dysfunction [50] .…”

Section: Exercise Arterial Function and Cardiac Rehabilitationmentioning

confidence: 99%

Exploring Vascular Function Biomarkers: Implications for Rehabilitation

Phillips¹,

Andaku²,

Mendes³

et al. 2017

Braz J Cardiovasc Surg

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The endothelium plays an important role in maintaining vascular homeostasis and regulating blood vessel function. Endothelial function is considered an independent predictor for risk of future cardiovascular events in cardiovascular and non-cardiovascular patients, as well as a predictor for postoperative complications in cardiovascular surgery patients. Brachial artery flow-mediated dilation by high-resolution ultrasound is widely used to evaluate endothelium-dependent vasodilation, which is mainly mediated by nitric oxide release. Physical exercise exerts beneficial effects on endothelial function and can be used in both primary and secondary prevention of cardiac and peripheral artery diseases, even in the postoperative period of cardiovascular surgery.

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Improved arterial flow-mediated dilation after exertion involves hydrogen peroxide in overweight and obese adults following aerobic exercise training

Abstract: Aerobic exercise prevents acute exertion-induced arterial dysfunction in overweight and obese adults via a phenotypic switch from nitric oxide-mediated dilation at rest to a predominately H2O2-mediated dilation after acute physical exertion.

Cited by 32 publications

References 40 publications

MicroRNA‐21 Contributes to Reduced Microvascular Function in Binge Drinking Young Adults

MicroRNA‐21 Contributes to Reduced Microvascular Function in Binge Drinking Young Adults

Nox2 contributes to hyperinsulinemia-induced redox imbalance and impaired vascular function

Exploring Vascular Function Biomarkers: Implications for Rehabilitation

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