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

Semin Nephrol. 2004 Mar;24(2):101-14. doi: 10.1016/j.semnephrol.2003.11.008.

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.

Publication types

  • Review

MeSH terms

  • Angiotensin II / administration & dosage
  • Angiotensin II / physiology*
  • Animals
  • Cells, Cultured
  • Chronic Disease
  • Disease Models, Animal
  • Humans
  • Hypertension / metabolism*
  • Infusion Pumps
  • Kidney Diseases / metabolism*
  • Oxidative Stress*
  • Sodium Chloride, Dietary / pharmacology

Substances

  • Sodium Chloride, Dietary
  • Angiotensin II