Cardiovascular diseases, including coronary artery disease and stroke, are the leading cause of death in the Western World (Rosamond et al., 2007). According to current medical theory, endothelial dysfunction is the primary cause of atherosclerosis, which is responsible for 90% of acute coronary syndrome and 80% of strokes (Mallika et al., 2007). Multiple factors affect endothelial function, but endothelial oxidative stress and low endothelial shear stress may be the most relevant (Davies, 2009, Thuillez and Richard, 2005). Flow mediated dilation (FMD) is considered a biomarker for endothelial function and brachial FMD is well correlated with coronary artery endothelial function.(Harris et al., 2010) However, the relationship between FMD and endothelial oxidative stress in vivo is still to be determined. Therefore, here we sought to determine if brachial artery FMD is associated with endothelial oxidative stress in humans. Twenty-three apparently healthy young men (25±4 yrs) with different activity background (e.g. sedentary, active recreational) underwent brachial artery FMD testing and venous endothelial cell biopsies on 2 occasions within 6 weeks. Protocol was approved by University of Florida Institutional Review Board. Immuno-fluorescence quantification was used to assess nitrotyrosine (NT), a criterion marker of endothelial oxidative stress. Values for NT expression were reported as a ratio of endothelial cell to human umbilical vein endothelial cell average pixel intensity. As shown on the figure, brachial FMD was inversely correlated with NT (R=0.273, p<0.05). The inverse relationship observed in the present study supports the hypothesis that FMD is associated with endothelial cell oxidative stress. Larger brachial dilations, relative to baseline vessel diameters, are associated with lower NT expression and vice versa. These results provide additional evidence to support the use of FMD as a non-invasive bio-marker for endothelial dysfunction.