Experimental evidence supports a pathogenic role of free radicals or reactive oxygen species (ROS) in the mechanism of hypertension. Indeed, vascular ROS produced in a controlled manner are considered important physiological mediators, functioning as signaling molecules to maintain vascular integrity by regulating endothelial function and vascular contraction‐relaxation. However, oxidative stress can be involved in the occurrence of endothelial dysfunction and related vascular injury. Thus, ROS activity could trigger pathophysiological cascades leading to inflammation, monocyte migration, lipid peroxidation, and increased deposition of extracellular matrix in the vascular wall, among other events. In addition, impairment of the antioxidant capacity associates with blood pressure elevation, indicating potential role of antioxidants as therapeutic antihypertensive agents. Nevertheless, although increased ROS biomarkers have been reported in patients with essential hypertension, the involvement of oxidative stress as a causative factor of human essential hypertension remains to be established. The aim of this chapter is to provide a novel insight into the mechanism of essential hypertension, including a paradigm based on the role played by oxidative stress.
Part of the book: Update on Essential Hypertension