African American (AA) race is an independent risk factor for vascular disease (e.g., hypertension) [1,2]. Hypertension disproportionately affects AAs, regardless of admixture [3], coupled with increased severity of hypertension and nearly a twofold increase in mortality associated with cardiovascular disease [4], thus revealing the epidemiological racial disparity and public health impact regarding hypertension [5,6]. Therefore, investigations are necessary to understand potential mechanism(s) that ultimately lead to premature and exacerbated hypertension-related cardiovascular diseases (e.g., stroke, kidney disease, hypertensive neuropathy, heart dysfunction) and end-organ failure in AA.Endothelial Dysfunction (EnDy), which can precede hypertension, has been shown to be greater in AA [7,8]. EnDy is characterized by a chronic low-grade inflammatory state of the endothelium and is marked by an exacerbated immune and oxidative stress response to inflammation. In vitro, Kalinowski et al. [1] showed that AA Human Umbilical Vein Endothelial Cells (HUVEC) exhibit EnDy marked by increased oxidative stress (e.g., superoxide and peroxynitrite production; Reactive Oxygen Species (ROS) and consequent reduced nitric oxide (NOx) bioavailability). Studies have previously shown that AA had significantly greater ROS in vitro and in vivo [9,10], and had greater circulating inflammatory endothelial microparticles (a novel biomarker of EnDy) [11,12]. One mechanistic explanation of these in vitro observations was that AA Endothelial Cells (EC) exhibited greater expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, increased basal inflammation, and lower antioxidant capacity [9] compared to Caucasian (CA) HUVEC that significantly improved in response to in vitro exercise mimetic (i.e., laminar shear stress)