Oxidative Stress in Hypertension and Chronic Kidney Disease: Role of Angiotensin II

Rajiv Agarwal, Ruth C. Campbell, David G. Warnock

Research output: Contribution to journalArticlepeer-review

81 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)101-114
Number of pages14
JournalSeminars in Nephrology
Volume24
Issue number2
DOIs
StatePublished - Mar 2004

ASJC Scopus subject areas

  • Nephrology

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