Dietary nitrate, nitric oxide, and restenosis
John P. Cooke, Yohannes T. Ghebremariam
John P. Cooke, Yohannes T. Ghebremariam
Published March 23, 2011
Citation Information: J Clin Invest. 2011;121(4):1258-1260. https://doi.org/10.1172/JCI57193.
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Commentary

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

John P. Cooke, Yohannes T. Ghebremariam

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Figure 1

Dietary nitrite and nitrate are absorbed in the gastrointestinal tract.

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Dietary nitrite and nitrate are absorbed in the gastrointestinal tract. ...
Plasma nitrate is concentrated in the salivary gland and undergoes reduction by bacteria in the mouth to nitrite. Salivary nitrate is converted in the stomach to nitrous acid, which may undergo spontaneous degradation to NO or which may nitrosylate proteins in the gut mucosa. Gastric NO is protective of the gut mucosa. Plasma nitrite may be converted by XOR in the vessel wall to produce vascular NO, which has homeostatic actions that preserve vessel patency. HNO2, nitrous acid; NO2–, nitrite; NO3–, nitrate; RSNO, S-nitrosothiol–containing peptide or protein.