Short-term regular aerobic exercise reduces oxidative stress produced by acute in the adipose microvasculature

Austin T. Robinson, Ibra S. Fancher, Varadarajan Sudhahar, Jing Tan Bian, Marc D. Cook, Abeer M. Mahmoud, Mohamed M. Ali, Masuko Ushio-Fukai, Michael D. Brown, Tohru Fukai, Shane A. Phillips

Research output: Contribution to journalArticle

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Abstract

High blood pressure has been shown to elicit impaired dilation in the vasculature. The purpose of this investigation was to elucidate the mechanisms through which high pressure may elicit vascular dysfunction and determine the mechanisms through which regular aerobic exercise protects arteries against high pressure. Male C57BL/6J mice were subjected to 2 wk of voluntary running (~6 km/day) for comparison with sedentary controls. Hindlimb adipose resistance arteries were dissected from mice for measurements of flow-induced dilation (FID; with or without high intraluminal pressure exposure) or protein expression of NADPH oxidase II (NOX II) and superoxide dismutase (SOD). Microvascular endothelial cells were subjected to high physiological laminar shear stress (20 dyn/cm2) or static condition and treated with ANG II pharmacological inhibitors. Cells were analyzed for the detection of ROS or collected for Western blot determination of NOX II and SOD. Resistance arteries from exercised mice demonstrated preserved FID after high pressure exposure, whereas FID was impaired in control mouse arteries. Inhibition of ANG II or NOX II restored impaired FID in control mouse arteries. High pressure increased superoxide levels in control mouse arteries but not in exercise mouse arteries, which exhibited greater ability to convert superoxide to H2O2. Arteries from exercised mice exhibited less NOX II + protein expression, more SOD isoform expression, and less sensitivity to ANG II. +Endothelial cells subjected to laminar shear stress exhibited less NOX II subunit expression. In conclusion, aerobic exercise prevents high pressure-induced vascular dysfunction through an improved redox environment in the adipose microvasculature. NEW & NOTEWORTHY We describe potential mechanisms contributing to aerobic exercise-conferred protection against high intra-vascular pressure. Subcutaneous adipose microvessels from exercise mice express less NADPH oxidase (NOX) II and more superoxide dismutase (SOD) and demonstrate less sensitivity to ANG II. In microvascular endothelial cells, shear stress reduced NOX II but did not influence SOD expression.

Original languageEnglish (US)
Pages (from-to)H896-H906
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume312
Issue number5
DOIs
StatePublished - May 2017

Fingerprint

Microvessels
NADPH Oxidase
Oxidative Stress
Arteries
Exercise
Pressure
Superoxide Dismutase
Blood Vessels
Endothelial Cells
Superoxides
Dilatation
Hindlimb
Inbred C57BL Mouse
Running
Oxidation-Reduction
Protein Isoforms
Proteins
Western Blotting
Pharmacology
Hypertension

Keywords

  • Endothelium
  • Exercise
  • Hypertension
  • Microcirculation
  • Oxidative stress

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Short-term regular aerobic exercise reduces oxidative stress produced by acute in the adipose microvasculature. / Robinson, Austin T.; Fancher, Ibra S.; Sudhahar, Varadarajan; Bian, Jing Tan; Cook, Marc D.; Mahmoud, Abeer M.; Ali, Mohamed M.; Ushio-Fukai, Masuko; Brown, Michael D.; Fukai, Tohru; Phillips, Shane A.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 312, No. 5, 05.2017, p. H896-H906.

Research output: Contribution to journalArticle

Robinson, Austin T. ; Fancher, Ibra S. ; Sudhahar, Varadarajan ; Bian, Jing Tan ; Cook, Marc D. ; Mahmoud, Abeer M. ; Ali, Mohamed M. ; Ushio-Fukai, Masuko ; Brown, Michael D. ; Fukai, Tohru ; Phillips, Shane A. / Short-term regular aerobic exercise reduces oxidative stress produced by acute in the adipose microvasculature. In: American Journal of Physiology - Heart and Circulatory Physiology. 2017 ; Vol. 312, No. 5. pp. H896-H906.
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abstract = "High blood pressure has been shown to elicit impaired dilation in the vasculature. The purpose of this investigation was to elucidate the mechanisms through which high pressure may elicit vascular dysfunction and determine the mechanisms through which regular aerobic exercise protects arteries against high pressure. Male C57BL/6J mice were subjected to 2 wk of voluntary running (~6 km/day) for comparison with sedentary controls. Hindlimb adipose resistance arteries were dissected from mice for measurements of flow-induced dilation (FID; with or without high intraluminal pressure exposure) or protein expression of NADPH oxidase II (NOX II) and superoxide dismutase (SOD). Microvascular endothelial cells were subjected to high physiological laminar shear stress (20 dyn/cm2) or static condition and treated with ANG II pharmacological inhibitors. Cells were analyzed for the detection of ROS or collected for Western blot determination of NOX II and SOD. Resistance arteries from exercised mice demonstrated preserved FID after high pressure exposure, whereas FID was impaired in control mouse arteries. Inhibition of ANG II or NOX II restored impaired FID in control mouse arteries. High pressure increased superoxide levels in control mouse arteries but not in exercise mouse arteries, which exhibited greater ability to convert superoxide to H2O2. Arteries from exercised mice exhibited less NOX II + protein expression, more SOD isoform expression, and less sensitivity to ANG II. +Endothelial cells subjected to laminar shear stress exhibited less NOX II subunit expression. In conclusion, aerobic exercise prevents high pressure-induced vascular dysfunction through an improved redox environment in the adipose microvasculature. NEW & NOTEWORTHY We describe potential mechanisms contributing to aerobic exercise-conferred protection against high intra-vascular pressure. Subcutaneous adipose microvessels from exercise mice express less NADPH oxidase (NOX) II and more superoxide dismutase (SOD) and demonstrate less sensitivity to ANG II. In microvascular endothelial cells, shear stress reduced NOX II but did not influence SOD expression.",
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AU - Cook, Marc D.

AU - Mahmoud, Abeer M.

AU - Ali, Mohamed M.

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