Seminars in Nephrology
Volume 24, Issue 2 , Pages 101-114, March 2004

Oxidative stress in hypertension and chronic kidney disease: role of angiotensin II1

  • Rajiv Agarwal

      Affiliations

    • Indiana University School of Medicine and Richard L. Roudebush VA Medical Center, Indianapolis, IN, USA
    • Corresponding Author InformationAddress reprint requests to Rajiv Agarwal, MD, Associate Professor of Clinical Medicine, Division of Nephrology, Department of Medicine, Indiana University and RLR VA Medical Center, 1481 West 10th Street, 111N, Indianapolis, IN 46202 USA
    • ,
  • Ruth C Campbell

      Affiliations

    • University of Alabama at Birmingham, Birmingham, AL, USA
    • ,
  • David G Warnock

      Affiliations

    • University of Alabama at Birmingham, Birmingham, AL, USA

Abstract 

Angiotensin II, via the type 1 (AT1) receptor, stimulates oxidative stress. The vasculature, interstitium, juxtaglomerular apparatus, and the distal nephron in the kidney express nicotinamide adenine dinucleotide phosphate (NADPH) oxidase that generates superoxide anion, which is an important component of angiotensin II-induced oxidative stress. The angiotensinogen gene is stimulated by NF-kappaB activation, which is sensitive to the redox ratio, providing a positive feedback loop that can upregulate angiotensin II production. Oxidative stress can accompany hypertension in many models, including the spontaneously hypertensive rat (SHR), angiotensin II-infused rats, renovascular hypertension, and the deoxycorticosterone acetate (DOCA) salt model of hypertension. AT1 receptor antagonists can abrogate the effects of angiotensin II on oxidative stress, thus providing an important mechanistic insight onto the renal protective effects of these agents in conditions associated with angiotensin II excess.

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  • 1 This is a US government work. There are no restrictions on its use.

PII: S0270-9295(03)00198-0

doi:10.1016/j.semnephrol.2003.11.008

Seminars in Nephrology
Volume 24, Issue 2 , Pages 101-114, March 2004

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