Acute oxidative stress attenuates endothelium-dependent vasodilation in mouse superior epigastric arteries

Endothelium-dependent control of microvessel diameter is important for controlling local blood flow in response to tissues metabolic needs. Excessive production of reactive oxygen species (ROS), as seen in some disease states, can interfere with normal Ca2+ signaling in endothelial cells. The focus of this study was to investigate the effects of hydrogen peroxides (H2O2), a form of acute oxidative stress, on endothelium-dependent vasodilation in mouse superior epigastric arteries (SEA). Prior to investigating the effects of oxidative stress, it was determined that vessels, at different transmural pressures, had a variable degree of myogenic tone. The amount of tone was investigated by measuring the passive vessel diameter (0 Ca2+) and the active vessel diameter (2 mM Ca2+). To test the effects of acute oxidative stress on vasodilation, isolated SEAs were pressurized at 80 mmHg while in a 2 mM Ca2+ physiological salt solution (PSS) containing 1 μM phenylephrine (PE) and diameter changes in response to increasing concentrations of acetylcholine (ACh) were measured. The percent dilation of the treatment group (n=3), which received 200 μM H2O2, was compared to the percent dilation of the control group (n=3). The results of this study show that H2O2 attenuates vasodilation in vessels precontracted with PE. The results suggest that high levels of ROS affect endotheliumdependent vasodilation