Abstract
Abstract The circulating anion nitrite, once thought to be a physiologically inert byproduct of nitric oxide (NO) oxidation, has been proposed to be a vascular storage form of bioactive NO. Nitrite is reduced to bioactive NO along a physiological oxygen and pH gradient by its reaction with deoxygenated hemoglobin and other hemoproteins. Through this mechanism, nitrite plays a role in hypoxic vasodilation and is capable of inhibiting mitochondrial respiration during hypoxia. Accumulating data demonstrate that nitrite is a potent mediator of cytoprotection after ischemia/reperfusion (I/R) injury in several organs, including the heart, liver, and brain. However, the mechanisms of nitrite-dependent cytoprotection remain unknown. In this article, we review the role of nitrite as a hypoxic source of NO and discuss the potential mechanisms of nitrite-mediated cytoprotection from I/R injury.
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