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1 NHLBI, NIH, Bethesda, Maryland, United States
2 Bethesda, Maryland, United States; NHLBI, NIH, Bethesda, Maryland, United States
3 CC, NIH, Bethesda, Maryland, United States
4 Biophysics Research Institute, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
5 Physics, Wake Forest University, Winston-Salem, North Carolina, United States
6 Pathology, University of Alabama at Birmingham, Birmingham, Alabama, United States
* To whom correspondence should be addressed. E-mail: mgladwin{at}nhlbi.nih.gov.
Accumulating evidence suggests that the simple and ubiquitous anion salt, nitrite (NO2-), is a physiological signaling molecule, with potential roles in intravascular endocrine nitric oxide (NO) transport, hypoxic vasodilation, signaling, and cytoprotection following ischemia-reperfusion. Human and animal studies of nitrite treatment and NO gas inhalation provide evidence that nitrite mediates many of the systemic therapeutic effects of NO gas inhalation, including peripheral vasodilation and prevention of ischemia-reperfusion-mediated tissue infarction. With regards to nitrite-dependent hypoxic signaling, biochemical and physiological studies suggest that hemoglobin possesses an allosterically regulated nitrite reductase activity that reduces nitrite to NO along the physiological oxygen gradient, potentially contributing to hypoxic vasodilation. An expanded consideration of nitrite as a hypoxia-dependent intrinsic signaling molecule has opened up a new field of research and therapeutic opportunities for diseases associated with regional hypoxia and vasoconstriction.
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