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Hypertension. 2006;48:828-829
Published online before print October 2, 2006, doi: 10.1161/01.HYP.0000242927.24428.25
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(Hypertension. 2006;48:828.)
© 2006 American Heart Association, Inc.


Editorial Commentaries

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

You-Lin Tain; Chris Baylis

From the Department of Physiology and Functional Genomics, University of Florida, Gainesville, Fla.

Correspondence to Chris Baylis, Department of Physiology and Functional Genomics, 1600 SW Archer Rd, PO Box 100274, University of Florida, Gainesville, FL 32610–0274. E-mail baylisc@ufl.edu


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

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 {approx}10 mm Hg, as well as an increase in renal vascular resistance and indices of increased oxidative stress. The BP measurements are made using the state-of-the-art technique, that is, telemetry, which allows detection of fairly . . . [Full Text of this Article]




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