Reactive Oxygen Species, NADPH Oxidases and Hypertension

• Type of Material: Article
• Authors: Srinivasa Raju Datla, Emory University; Kathy Griendling, Emory University
• Language: English
• Date: 2010-09
• Publisher: American Heart Association
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2010 American Heart Association, Inc.
• Final Published Version (URL): http://hyper.ahajournals.org/content/56/3/325
• Title of Journal or Parent Work: Hypertension
• ISSN: 0194-911X
• Volume: 56
• Issue: 3
• Start Page: 325
• End Page: 330
• Grant/Funding Information: This work was supported by National Institutes of Health Grants HL38206, HL092120 and HL095070.; National Heart, Lung, and Blood Institute : NHLBI
• Research Categories: Health Sciences, General

Abstract

Reactive oxygen species (ROS) produced in the neuronal, renal and vascular systems not only influence cardiovascular physiology, but are also strongly implicated in pathological signaling leading to hypertension. Different sources of ROS have been identified, ranging from xanthine-xanthine oxidase and mitochondria to NADPH oxidase (Nox) enzymes. Out of seven Nox family members, Nox1, Nox2, Nox4 (and Nox5 in humans) influence the cardiovascular system. Their activation processes, cell and tissue distribution vary widely, adding complexity to understanding their functional roles. Whether these systems act collectively or independently in disease conditions is unclear, but recently, feed forward mechanisms have been established between ROS sources. Studies published in Hypertension over the last few years are the focus of this review and they provide a framework with which to consider the roles of Nox enzymes in neuronal, renal and vascular hypertensive mechanisms, as well as cardiac remodeling, and their relationships with other ROS-generating systems.