title: Short-term regular aerobic exercise reduces oxidative stress produced by acute in the adipose microvasculature.
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 H2O2Arteries 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 & NOTEWORTHYWe describe potential mechanisms contributing to aerobic exercise-conferred protection against high intravascular 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.
authors.affiliation: Department of Physical Therapy, University of Illinois at Chicago, Chicago, Illinois; shanep@uic.edu.|Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois.|Integrative Physiology Laboratory, University of Illinois at Chicago, Chicago, Illinois.
authors.forename: Austin T
authors.initials: AT
authors.lastname: Robinson
authors.affiliation: Department of Physical Therapy, University of Illinois at Chicago, Chicago, Illinois.|Division of Pulmonary, Critical Care, Sleep, and Allergy, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois.
authors.forename: Ibra S
authors.initials: IS
authors.lastname: Fancher
authors.affiliation: Departments of Medicine (Section of Cardiology) and Pharmacology, Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, Illinois.|Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois.
authors.forename: Varadarajan
authors.initials: V
authors.lastname: Sudhahar
authors.affiliation: Department of Physical Therapy, University of Illinois at Chicago, Chicago, Illinois.
authors.forename: Jing Tan
authors.initials: JT
authors.lastname: Bian
authors.affiliation: Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois.|Integrative Physiology Laboratory, University of Illinois at Chicago, Chicago, Illinois.
authors.forename: Marc D
authors.initials: MD
authors.lastname: Cook
authors.affiliation: Department of Physical Therapy, University of Illinois at Chicago, Chicago, Illinois.|Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois.|Integrative Physiology Laboratory, University of Illinois at Chicago, Chicago, Illinois.
authors.forename: Abeer M
authors.initials: AM
authors.lastname: Mahmoud
authors.affiliation: Department of Physical Therapy, University of Illinois at Chicago, Chicago, Illinois.|Integrative Physiology Laboratory, University of Illinois at Chicago, Chicago, Illinois.
authors.forename: Mohamed M
authors.initials: MM
authors.lastname: Ali
authors.affiliation: Departments of Medicine (Section of Cardiology) and Pharmacology, Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, Illinois.
authors.forename: Masuko
authors.initials: M
authors.lastname: Ushio-Fukai
authors.affiliation: Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois.|Integrative Physiology Laboratory, University of Illinois at Chicago, Chicago, Illinois.
authors.forename: Michael D
authors.initials: MD
authors.lastname: Brown
authors.affiliation: Departments of Medicine (Section of Cardiology) and Pharmacology, Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, Illinois.|Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois.
authors.forename: Tohru
authors.initials: T
authors.lastname: Fukai
authors.affiliation: Department of Physical Therapy, University of Illinois at Chicago, Chicago, Illinois; shanep@uic.edu.|Integrative Physiology Laboratory, University of Illinois at Chicago, Chicago, Illinois.|Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois; and.
authors.forename: Shane A
authors.initials: SA
authors.lastname: Phillips
mesh_terms: D000273:Adipose Tissue / Q000098:blood supply* / Q000502:physiology*; D057912:Angiotensin II Type 2 Receptor Blockers / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D042783:Endothelial Cells / Q000187:drug effects; D015444:Exercise / Q000502:physiology*; D006614:Hindlimb / Q000098:blood supply; D006801:Humans; D008297:Male; D008562:Membrane Glycoproteins / Q000037:antagonists & inhibitors / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D055806:Microvessels / Q000502:physiology*; D000074662:NADPH Oxidase 2; D019255:NADPH Oxidases / Q000037:antagonists & inhibitors / Q000235:genetics; D018384:Oxidative Stress / Q000502:physiology*; D013482:Superoxide Dismutase / Q000037:antagonists & inhibitors / Q000235:genetics; D014655:Vascular Resistance
chemical_list: D057912:Angiotensin II Type 2 Receptor Blockers; D008562:Membrane Glycoproteins; D013482:Superoxide Dismutase; C488842:Cybb protein, mouse; D000074662:NADPH Oxidase 2; D019255:NADPH Oxidases
keywords: endothelium; exercise; hypertension; microcirculation; oxidative stress