title: Dietary nitrate, nitric oxide, and restenosis.
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.
authors: Stanford Cardiovascular Institute, Stanford, California 94305, USA.
authors: John P
authors: JP
authors: Cooke
authors: Yohannes T
authors: YT
authors: Ghebremariam
mesh_terms: D000818:Animals; D023903:Coronary Restenosis / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D004032:Diet; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D006706:Homeostasis; D006965:Hyperplasia; D051379:Mice; D008954:Models, Biological; D009566:Nitrates / Q000008:administration & dosage*; D009569:Nitric Oxide / Q000378:metabolism*; D009573:Nitrites / Q000008:administration & dosage; D017539:Tunica Intima / Q000293:injuries / Q000473:pathology
chemical_list: D009566:Nitrates; D009573:Nitrites; D009569:Nitric Oxide