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(Hypertension. 2007;50:600.)
© 2007 American Heart Association, Inc.

Editorial Commentaries

The Continuing Saga of Neuronal Oxidative Stress in Hypertension

Nox, Nox–Who’s There, and Where?

Mark W. Chapleau

From the Departments of Internal Medicine and Molecular Physiology and Biophysics and the Cardiovascular Center, University of Iowa Carver College of Medicine, and the Veterans Affairs Medical Center, Iowa City.

Correspondence to Mark W. Chapleau, University of Iowa Carver College of Medicine, 629 MRC, 200 Hawkins Dr, Iowa City, IA 52242. E-mail mark-chapleau@uiowa.edu

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

	Introduction

 
Numerous studies have demonstrated increased production of reactive oxygen species (ROS) in blood vessels and kidneys in hypertension and provided evidence that the oxidative stress in these organs causes or contributes to the elevated blood pressure.^1,2 Recently, the nervous system has emerged as an additional site and target of oxidative stress in hypertension. The vast majority of these studies have focused on the central nervous system, where activation of reduced nicotinamide-adenine dinucleotide phosphate [NAD(P)H] oxidase has been shown to contribute to sympatho-excitation and increases in blood pressure.³

NAD(P)H oxidase is a major source of ROS in hypertension, in both peripheral tissues and brain^1–3; and homologues of NAD(P)H oxidase (Nox) are differentially expressed in diverse cell types including neurons.^3,4 NAD(P)H oxidase consists of 2 membrane-bound subunits (p22^phox and Nox) and cytosolic components that are recruited to the membrane during activation (p47^phox, p67^phox, p40^phox, and GTPase Rac).⁴ Nox homologues include Nox1, Nox2 (gp91^phox), Nox3, Nox4, Nox5, Duox1, and Duox2.⁴

	Is NAD(P)H Oxidase Upregulated in the Peripheral Nervous System in Hypertension?

 
Neurohumoral regulation of arterial blood pressure is of course not only determined by the central nervous system but is also influenced by alterations in sensory nerve activity and the function of peripheral sympathetic and parasympathetic nerves. The article by Cao et al,⁵ published in this issue of Hypertension, is one of a series of articles from this group^6–8 that describe NAD(P)H oxidase expression and regulation of ROS production in sympathetic neurons located in prevertebral sympathetic ganglia of normotensive and hypertensive (deoxycorticosterone acetate [DOCA]–salt) rats. The present results . . . [Full Text of this Article]

Related Article:

Differential Regulation of NADPH Oxidase in Sympathetic and Sensory Ganglia in Deoxycorticosterone Acetate–Salt Hypertension

Xian Cao, Xiaoling Dai, Lindsay M. Parker, and David L. Kreulen
Hypertension 2007 50: 663-671. [Abstract] [Full Text] [PDF]