Dietary nitrate, nitric oxide, and restenosis

J Clin Invest. 2011 Apr;121(4):1258-60. doi: 10.1172/JCI57193. Epub 2011 Mar 23.


Endothelium-derived NO controls the contractility and growth state of the underlying vascular smooth muscle cells and regulates the interaction of the vessel wall with circulating blood elements. Acute injury of the vessel wall denudes the endothelial lining, removing homeostatic regulation and precipitating a wave of events leading to myointimal hyperplasia. In this issue of the JCI, Alef and colleagues provide evidence that in the injured vessel wall, the disruption of the NOS pathway is countered by induction of xanthine oxidoreductase, an enzyme capable of producing NO from nitrite. In addition, they link low dietary nitrite levels to increased severity of myointimal hyperplasia following vessel injury in mice.

Publication types

  • Comment
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Coronary Restenosis / etiology*
  • Coronary Restenosis / metabolism*
  • Coronary Restenosis / pathology
  • Diet
  • Endothelium, Vascular / metabolism
  • Endothelium, Vascular / pathology
  • Homeostasis
  • Hyperplasia
  • Mice
  • Models, Biological
  • Nitrates / administration & dosage*
  • Nitric Oxide / metabolism*
  • Nitrites / administration & dosage
  • Tunica Intima / injuries
  • Tunica Intima / pathology


  • Nitrates
  • Nitrites
  • Nitric Oxide