Oxidative stress and vascular function: implications for pharmacologic treatments.

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Abstract

Production of considerable amounts of reactive oxygen species (ROS) eventually leads to oxidative stress. A key role of oxidative stress is evident in the pathologic mechanisms of endothelial dysfunction and associated cardiovascular diseases. Vascular enzymes such as NADPH oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase are involved in the production of ROS. The question remains whether pharmacologic approaches can effectively combat the excessive ROS production in the vasculature. Interestingly, existing registered cardiovascular drugs can directly or indirectly act as antioxidants, thereby preventing the damaging effects of ROS. Moreover, new compounds targeting NADPH oxidases have been developed. Finally, food-derived compounds appear to be effective inhibitors of oxidative stress and preserve vascular function.
Original languageEnglish
Pages (from-to)154-161
Number of pages8
JournalCurrent Hypertension Reports
Volume12
Issue number3
DOIs
Publication statusPublished - Jun 2010

Keywords

  • Hypertension
  • Vasculature
  • Antioxidant
  • NADPH oxidase
  • Xanthine oxidase
  • eNOS
  • NO
  • Reactive oxygen species
  • ROS
  • Oxidative stress
  • Flavonoids
  • Polyphenols
  • Antihypertensive drugs
  • NOX
  • Oxygen radicals
  • XANTHINE-OXIDASE
  • NADPH OXIDASES
  • IN-VIVO
  • MOLECULAR-MECHANISMS
  • SUPEROXIDE-DISMUTASE
  • ISCHEMIA-REPERFUSION
  • LIPID-PEROXIDATION
  • ARGINASE ACTIVITY
  • BLOOD-PRESSURE
  • NOX FAMILY

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