Dietary nitrate, nitric oxide, and restenosis. uri icon

Overview

abstract

  • 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 date

  • March 23, 2011

Research

keywords

  • Coronary Restenosis
  • Nitrates
  • Nitric Oxide

Identity

PubMed Central ID

  • PMC3069795

Scopus Document Identifier

  • 79953315574

Digital Object Identifier (DOI)

  • 10.2134/jeq2007.0177

PubMed ID

  • 21436578

Additional Document Info

volume

  • 121

issue

  • 4