This Article Full Text Full Text (PDF) All Versions of this Article: 48/2/309    most recent 01.HYP.0000231307.69761.2ev1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ye, S. Articles by Campese, V. M. Search for Related Content PubMed PubMed Citation Articles by Ye, S. Articles by Campese, V. M. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB PHENOL Related Collections Animal models of human disease Other hypertension

(Hypertension. 2006;48:309.)
© 2006 American Heart Association, Inc.

Original Articles

Oxidative Stress Mediates the Stimulation of Sympathetic Nerve Activity in the Phenol Renal Injury Model of Hypertension

From the Division of Nephrology and the Hypertension Center, Keck School of Medicine, University of Southern California, Los Angeles.

Correspondence to Vito M. Campese, Division of Nephrology, and Hypertension Center, Keck School of Medicine, University of Southern California, 1200 North State St, Los Angeles, CA 90033. E-mail campese{at}usc.edu

Renal injury caused by the injection of phenol in the lower pole of one kidney increases blood pressure (BP), norepinephrine secretion from the posterior hypothalamic nuclei (PH), and renal sympathetic nerve activity in the rat. Renal denervation prevents these effects of phenol. We have also demonstrated that noradrenergic traffic in the brain is modulated by NO and interleukin-1ß. In this study, we tested the hypothesis that the increase in sympathetic nervous system (SNS) activity in the phenol renal injury model is because of activation of reactive oxygen species. To this end, first we examined the abundance of several components of reduced nicotinamide-adenine dinucleotide phosphate oxidase (identified as the major source of reactive oxygen species), including gp91phox/Nox2, p22phox, p47phox, and Nox3 using real-time PCR. Second, we evaluated the effects of 2 superoxide dismutase mimetic, tempol (4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl), and superoxide dismutase-polyethylene glycol on central and peripheral SNS activation caused by intrarenal phenol injection. Intrarenal injection of phenol raised BP, NE secretion from the PH, renal sympathetic nerve activity, and the abundance of reduced nicotinamide-adenine dinucleotide phosphate and reduced the abundance of interleukin-1ß and neural-NO synthase mRNA in the PH, paraventricular nuclei, and locus coeruleus compared with control rats. When tempol or superoxide dismutase-polyethylene glycol were infused in the lateral ventricle before phenol, the effects of phenol on BP and SNS activity were abolished. The studies suggest that central activation of the SNS in the phenol-renal injury model is mediated by increased reactive oxygen species in brain nuclei involved in the noradrenergic control of BP.

Key Words: hypertension, renal • sympathetic nervous system • nitric oxide • interleukins • oxidative stress

This article has been cited by other articles:

				X. Chen, K. Patel, S. G. Connors, M. Mendonca, W. J. Welch, and C. S. Wilcox Acute antihypertensive action of Tempol in the spontaneously hypertensive rat Am J Physiol Heart Circ Physiol, December 1, 2007; 293(6): H3246 - H3253. [Abstract] [Full Text] [PDF]