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. Methods: Male C57Bl6 mice were subjected to two weeks of voluntary running (~ 6km/day) for comparison to sedentary controls. Hind limb adipose resistance arteries were dissected from mice for measurement 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 dynes/cm2) or static condition and treated with angiotensin II (ang II) + pharmacologic inhibitors. Cells were analyzed for detection of reactive oxygen species determination of NOX II and SOD protein. Results: Exercise mice resistance arteries demonstrated preserved FID following high pressure exposure, whereas FID was impaired in control mice arteries. Inhibition of ang II or NOX II restored FID in control mice arteries. High pressure increased superoxide levels in control mice arteries, but not in exercise mice arteries, which exhibited greater ability to convert superoxide to hydrogen peroxide. Arteries from exercise 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. Conclusion: Aerobic exercise prevents high pressure-induced vascular dysfunction through an improved redox environment in the adipose microvasculature.
- oxidative stress
- Copyright © 2016, American Journal of Physiology-Heart and Circulatory Physiology