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The article “Role of extracellular superoxide dismutase in the mouse angiotensin slow pressor response” describes studies in EC-SOD knockout and wild-type mice by Welch et al.1 This study is a continuation of a series of investigations by these researchers who have advanced our understanding of the role of reactive oxygen species (ROS) in the pathogenesis of hypertension. Of particular note, this group combines sophisticated physiological measurements (renal hemodynamics and conscious blood pressure [BP] by telemetry) with in vitro measures of protein and mRNA expression, as well as markers of oxidative stress.There is clear evidence that increased oxidative stress is both a cause and a consequence of hypertension.2,3 Oxidative stress means that an imbalance develops between the pro-oxidant and antioxidant systems, with increased ROS generation and/or decreased antioxidant capacity. There are many oxidases responsible for ROS production and many antioxidant defenses, in both intracellular and extracellular locations. Dissecting the role of individual players is quite difficult, because, for example, there are 3 species of SOD, including EC-SOD, but no selective EC-SOD inhibitors are available. This study exploits the availability of the EC-SOD knockout mice to investigate the importance of this enzyme in BP control.One novel observation in this study is the demonstration that young adult EC-SOD knockout mice exhibit an elevated baseline BP of ≈10 mm Hg, as well as an increase in renal vascular resistance and …

Dissecting the Causes of Oxidative Stress in an In Vivo Model of Hypertension