Interactions of angiotensin II with NAD(P)H oxidase, oxidant stress and cardiovascular disease

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David G Harrison1, Hua Cai, Ulf Landmesser

  • 1Division of Caridology, Emory University, Atlanta, Georgia 30322, USA. dharr02@emory.edu

Journal of the Renin-Angiotensin-Aldosterone System : JRAAS
|June 14, 2003
PubMed

Insights

Elevated angiotensin II (Ang II) activates NAD(P)H oxidase, increasing reactive oxygen species (ROS). This contributes to cardiovascular diseases like hypertension and atherosclerosis, highlighting NAD(P)H oxidase as a therapeutic target.

Area of Science:

  • Cardiovascular Biology
  • Oxidative Stress Research
  • Molecular Medicine

Background:

  • Elevated angiotensin II (Ang II) is implicated in numerous cardiovascular diseases, including hypertension, hypercholesterolemia, atherosclerosis, left ventricular hypertrophy (LVH), heart failure, and diabetes.
  • Ang II significantly activates NAD(P)H oxidase, a primary source of reactive oxygen species (ROS) in vascular cells.

Discussion:

  • Increased cellular ROS production by NAD(P)H oxidase contributes to vascular disease pathogenesis.
  • ROS alters endothelial function, promotes smooth muscle cell growth, stimulates inflammatory mediators, and modulates matrix remodeling.

Key Insights:

  • Studies in genetically modified mice demonstrate Ang II-induced NAD(P)H oxidase activation contributes to hypertension, LVH, and atherosclerosis.
  • Growing evidence links NAD(P)H oxidase activity to human cardiovascular diseases.

Outlook:

  • NAD(P)H oxidase emerges as a promising therapeutic target for cardiovascular diseases.
  • Further research is warranted to explore and validate NAD(P)H oxidase inhibitors for clinical application.

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