Journal
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-MOLECULAR & INTEGRATIVE PHYSIOLOGY
Volume 142, Issue 2, Pages 130-135Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cbpb.2005.04.016
Keywords
nitric oxide; nitrite; hemoglobin; soluble guanylate cyclase; red blood cell; vasodilation; hypoxia; diffusion; computer simulation
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Funding
- NHLBI NIH HHS [R01 HL058091, HL58091, HL70146] Funding Source: Medline
- NIGMS NIH HHS [GM55792] Funding Source: Medline
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Nitrite has long been known to be vasoactive when present at large concentrations but it was thought to be inactive under physiological conditions. Surprisingly, we have recently shown that supraphysiological and near physiological concentrations of nitrite cause vasodilation in the human circulation. These effects appeared to result from reduction of nitrite by deoxygenated hemoglobin. Thus, nitrite was proposed to play a role in hypoxic vasodilation. We now discuss these results in the context of nitrite reacting with hemoglobin and effecting vasodilation and present new data modeling the nitric oxide (NO) export from the red blood cell and measurements of soluble guanylate cyclase (sGC) activation. We conclude that NO generated within the interior of the red blood cell is not likely to be effectively exported directly as nitric oxide. Thus, an intermediate species must be formed by the nitrite/deoxyhemoglobin reaction that escapes the red cell and effects vasodilation. (C) 2005 Elsevier Inc. All rights reserved.
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