Increasing evidence implicates reactive oxygen species in the pathogenesis of hypertension and its cardiovascular complications. By altering the balance in the endothelium between vasoconstrictors such as thromboxane and isoprostanes and vasodilators such as nitric oxide, reactive oxygen species contribute to endothelium-dependent contractions and increased vascular resistance. Antioxidants can restore endothelial function and decrease blood pressure in several models of hypertension and in some, but not all, studies of humans with essential hypertension. The potential of antioxidant therapy for hypertension is considerable.