An oxidative stress is a result of an imbalance between pro- and antioxidants, and leads to several alterations on subcellular level, and therefore may be involved in aging and numerous pathological disorders. The aim of this review of literature was to present current knowledge on contribution of free radicals in pathogenesis of essential hypertension. The sources of free radicals in vascular system are NADH/NAD(P)H oxidases, xanthine oxidase, nitric oxide synthase, cyclooxygenase of endothelial cells, vascular myocytes, macrophages and neutrophiles. Free radicals cause destruction of cell membranes, intracellular Ca2+ overload, genome impairment, and deficit of energy. The reduced activity of nitric oxide found in arterial hypertension may be a result of either decreased synthesis or increased inactivation by superoxide anions, and contributes to endothelial dysfunction. Low activity of nitric oxide results in domination of vasoconstrictive activity such factors as angiotensin II, endothelin, prostaglandin H2 and thromboxane A2. Moreover, the deficit in nitric oxide seems to be partially responsible for deterioration of natriuresis. Recently, it has been revealed that free radicals are mediators of angiotensin’s as well as endothelin and bradykinin action. They act also as mediators of growth factors, through activation of protooncogens c-fos and c-jun, and therefore may contribute to hypertensive arterial wall remodeling. Some studies have demonstrated presence of positive relationship between blood pressure values and activity of enzyme, which are responsible for release of free radicals, or concentration of free radicals. Finally, the possibility of preventing vasoconstriction and arterial wall remodeling by antioxidants confirms partial contribution of free radicals in promoting vascular alterations. Although published studies don’t allow to consider free radicals as an proved reason of arterial hypertension, they evidence the contribution of free radicals in development of hypertension complications.