Journal of the American Society of Hypertension
Volume 1, Issue 4 , Pages 242-250, July 2007

A vitamin-E-fortified diet reduces oxidative stress, sympathetic nerve activity, and hypertension in the phenol-renal injury model in rats

  • Vito M. Campese, MD

      Affiliations

    • Corresponding Author InformationCorresponding author: Vito M. Campese, MD, Division of Nephrology, and Hypertension Center, Keck School of Medicine, USC, 1200 North State Street, Los Angeles, California 90033. Tel: 323-226-7307; fax: 323-226-5390.
  • ,
  • Shaohua Ye, MD

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

Received 9 March 2007; accepted 20 April 2007.

Abstract 

Renal injury caused by the injection of phenol in the lower pole of one kidney increases sympathetic nervous system (SNS) activity and blood pressure (BP), and these effects are mediated by increased reactive oxygen species (ROS) in brain nuclei involved in the noradrenergic control of BP. This suggests that therapy with antioxidants might be beneficial in this model. In this study, we tested the hypothesis that a vitamin (Vit)-E-enriched diet might decrease oxidative stress in the brain and result in reduced SNS activity and BP in animals with phenol-renal injury. To this end, we examined the effects of a Vit-E-fortified diet vs. a control diet on BP, norepinephrine (NE) secretion from the posterior hypothalamic nuclei (PH), and the abundance of several components of Nicotinamide Adenine Dinucleotide Phosphate (NADPH) oxidase in the brain of rats with phenol-induced renal injury. A Vit-E-fortified diet mitigated the formation of ROS in the brain, and this was associated with reduced SNS activity and BP in rats with phenol-induced renal injury. In conclusion, antioxidants appear to be beneficial in the management of hypertension caused by renal injury and increased SNS activity.

Keywords: Hypertension, renal injury, sympathetic nervous system, reactive oxygen species, vitamin E, nitric oxide, interleukin-1β

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 This study was supported by National Institutes of Health Grant R01 HL070027.Conflict of interest: none.

PII: S1933-1711(07)00090-3

doi:10.1016/j.jash.2007.04.003

Journal of the American Society of Hypertension
Volume 1, Issue 4 , Pages 242-250, July 2007