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- Roxana Loperena and David G Harrison.
- Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, 2220 Pierce Drive, Room 536 Robinson Research Building, Nashville, TN 37232, USA.
- Med. Clin. North Am. 2017 Jan 1; 101 (1): 169193169-193.
AbstractIt has become clear that reactive oxygen species (ROS) contribute to the development of hypertension via myriad effects. ROS are essential for normal cell function; however, they mediate pathologic changes in the brain, the kidney, and blood vessels that contribute to the genesis of chronic hypertension. There is also emerging evidence that ROS contribute to immune activation in hypertension. This article discusses these events and how they coordinate to contribute to hypertension and its consequent end-organ damage.Copyright © 2016 Elsevier Inc. All rights reserved.
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