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Nephrol Dial Transplant (2003) 18: 1439-1442
© 2003 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Oxidative stress: does it play a role in the genesis of essential hypertension and hypertension of uraemia?

Martin Tepel

Med. Klinik IV, Univ. Klinik Benjamin Franklin, Freie Universität Berlin, Germany

Correspondence and offprint requests to: Dr Martin Tepel, Med. Klinik IV, Univ.-Klinik Benjamin Franklin, Freie Universität Berlin, Hindenburgdamm 30, D-12200 Berlin, Germany. Email: tepel@zedat.fu-berlin.de

Keywords: essential hypertension; hypertension; oxidative stress; uraemia

The first 10% of the full text of this article appears below.

Reactive oxygen species: general aspects

Reactive oxygen species, including superoxide radicals, hydrogen peroxide, nitric oxide, peroxynitrite, hydroxyl radicals and hypochlorous acid are by-products of normal metabolic processes in cells. Reactive oxygen species can be found in several cells including macrophages and vascular smooth muscle cells. At low concentrations reactive oxygen species can act as physiological mediators of cellular responses whereas higher concentrations may cause cell damage [1,2]. The major sources of reactive oxygen species are leakages from the electron transport chains of mitochondria and endoplasmic reticulum. Cellular energy metabolism is based on the production of ATP through the electron transport reaction in which O2 accepts electrons and H+ and then is eventually reduced to water. Only 1–2% of the electrons are leaked to generate superoxide radicals in reactions mediated by coenzyme Q and ubiquinone and its complexes. During ageing (and probably in patients . . . [Full Text of this Article]

Reactive oxygen species and hypertension in the absence of renal failure

Reactive oxygen species and hypertension in uraemia


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