Oxidative stress, resultant from an imbalance of generation over degradation of the reactive oxygen species (ROS), contributes to the pathophysiology of cardiovascular diseases, including atherosclerosis, heart failure, and hypertension.Earlier studies from our laboratory revealed that in the rostral ventrolateral medulla (RVLM), where sympathetic premotor neurons reside, an increase in gene transcription and enzyme activity of the NADPH oxidase and dysfunction of mitochondrial electron transport chain (ETC) enzyme activity;alongside reductions in protein synthesis and enzyme activity of antioxidants that include superoxide dismutase (SOD) and mitochondrial uncoupling protein 2 (MtUCP2), contribute to the sustained increase in tissue levels of superoxide anion (O·-) and hydrogen peroxide (H2O2) in the spontaneously hypertensive rats (SHR).