Hypertension is considered the most important risk factor in the development ofcardiovascular disease. An increasing body of evidence suggests that oxidative stress,which results in an excessive generation of reactive oxygen species (ROS), plays a keyrole in the pathogenesis of hypertension. The modulation of the vasomotor systeminvolves ROS as mediators of vasoconstriction induced by angiotensin II, endothelin-1and urotensin-II, among other factors. The bioavailability of nitric oxide (NO), a majorvasodilator, is modulated by the cellular redox status. Under physiological conditions,low concentrations of intracellular ROS are important in normal redox signaling tomaintain vascular function and integrity. However, under pathological conditions, ROScontribute to vascular dysfunction and remodeling through oxidative injury. Increasedproduction of superoxide anion and hydrogen peroxide, decreased NO synthesis anddiminished antioxidant capacity have been found in patients with essential hypertension.Antioxidants are reducing agents that can neutralize these oxidative compounds, whichotherwise damage biomolecules and thereby cause functional and even structuralimpairment of the end-organs. The use of antioxidant vitamins such as vitamins C and Efor protection against vascular endothelial injury has gained considerable interest.Available data support the role of these vitamins as effective antioxidants to counteractthe effects of ROS. In this chapter, the following core hypothesis is evaluated: essentialhypertension is a manifestation of subtle vascular inflammation brought about byheightened oxidative stress. For this purpose, the mechanisms involved in the generation of vascular ROS are discussed, as well as the role of oxidative stress in the pathogenesisof hypertension. Possible therapeutic strategies to overcome the heightened oxidativestress in essential hypertension are suggested. © 2013 Nova Science Publishers, Inc. All rights reserved.