Angiotensin-induced inflammation and vascular injury


  • D.N. Mueller
  • R. Dechend
  • A. Fiebeler
  • J.K. Park
  • H. Haller
  • F.C. Luft


  • Contributions to Nephrology


  • Contrib Nephrol 135: 138-152


  • Hypertension, perhaps the most important risk factor for stroke, ischemic heart disease and progressive renal failure, is not commonly associated with inflammation. However, as the growing role of 'oxidative stress' as a component of many human disorders including hypertension becomes more appreciated, our impression of hypertension as a rather indolent, solely hemodynamic process is being revised. Reactive oxygen species are the end result of univalent reductions on oxygen resulting in the production of superoxide anion(O2), hydrogen peroxide (H2O2), and water (H2O). Reactive oxygen species influence both normal and abnormal cellular processes, including cellular growth, hypertrophy, remodeling, lipid oxidation, modulation of vascular tone, and inflammation. The notion that superoxide anion might have something to do with hypertenion was suggested over a decade ago. Reactive oxygen species can also act as intracellular signaling molecules in vascular cells controlling growth, survival and apoptosis. The specific response is dictated by the intracellular targets involved. The potential targets of reactive oxygen species in endothelial and vascular smooth muscle cells are extracellular signal-related kinases, stress activated protein kinases, caspases, nuclear factor-{kappa}B (NF-{kappa}B) and Akt kinase. NF-{kappa}B activation has been associated with vascular inflammation and cell survival. Akt is associated with the protective effects of shear stress, vascular endothelial growth factor-induced functions, and cell survival.