Oxygen radical stress in vascular disease: the role of endothelial nitric oxide synthase.
Impaired nitric oxide (NO) activity in proatherosclerotic states has been suggested to be caused mainly by increased degradation of NO by oxygen radicals. In recent years, endothelial NO synthase has been identified as a system that contributes to oxygen radical stress under pathophysiologic conditions. We discuss the origin of NO synthase-derived superoxide production, as well as possibilities to modulate (pathologic) shifts in NO/superoxide production by endothelial NO synthase.
Stroes
E S
ES
Department of Vascular Medicine, University Hospital Utrecht, The Netherlands.
van Faassen
E E
EE
van Londen
G J
GJ
Rabelink
T J
TJ
D000818:Animals; D004730:Endothelium, Vascular / Q000201:enzymology*; D006801:Humans; D009569:Nitric Oxide / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000502:physiology*; D052250:Nitric Oxide Synthase Type III; D017382:Reactive Oxygen Species / Q000502:physiology*; D013481:Superoxides / Q000378:metabolism; D014652:Vascular Diseases / Q000201:enzymology* / Q000503:physiopathology
D017382:Reactive Oxygen Species; D013481:Superoxides; D009569:Nitric Oxide; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III