Background: Disruption of redox signaling is a common pathophysiological mechanism
observed in several diseases. In hypertension, oxidative stress, resulted either from enhances in
Reactive Oxygen Species (ROS) production or decreases in antioxidant defenses, is associated with
increase in blood pressure, endothelial dysfunction and vascular remodeling. Although the role of
oxidative stress in the development of hypertension is well known, it is still unclear if this process is
a cause or a consequence of tissue changes in hypertension. Indeed, unbalanced ROS formation
results in several detrimental effects that contribute to hypertension, including reduction in nitric
oxide bioavailability and activation of metalloproteinases. Additionally, ROS may also directly
react with lipids, proteins and DNA, thereby contributing to tissue damage associated with hypertension.
Therefore, a deep understanding of the role of oxidative stress in hypertension is essential
to comprehend its pathophysiology and to identify new therapeutic targets.
Conclusion: This minireview discusses the main enzymatic sources of oxidants and the major antioxidant
defenses in the vasculature, followed by the effects of oxidative stress in hypertension,
highlighting endothelial dysfunction, vascular remodeling and tissue damage.