Abstract
Hypertension is a major cardiovascular risk factor. Of the many processes involved in the pathophysiology of hypertension, cardiac, vascular and renal damage due to oxidative stress (excess bioavailability of reactive oxygen species (ROS)) is important. Physiologically, ROS regulate cell function through redox-sensitive pathways. In hypertension, oxidative stress promotes endothelial dysfunction, vascular remodeling and inflammation, leading to vascular damage. While experimental evidence indicates a causative role for oxidative stress in hypertension, human data are less convincing. This may relate to sub-optimal approaches to accurately measure ROS in humans. Various methods have been developed to assess the extent and nature of oxidative stress, including markers of protein oxidation, lipid oxidation, and anti-oxidant status. These approaches are, in general, indirect and measure indices of redox state. While large clinical studies to establish whether biomarkers of oxidative stress accurately predict disease risk are still needed, oxidative biomarkers have provided important mechanistic insights regarding redox-sensitive processes of hypertension. Here we briefly describe the importance of ROS in redox signaling and hypertension and discuss biomarkers of oxidative stress in human hypertension.
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