Hemoglobin mediated nitrite activation of soluble guanylyl cyclase. Comp Biochem Physiol A Mol Integr Physiol 2005 Oct;142(2):130-5
Date
06/07/2005Pubmed ID
15936233DOI
10.1016/j.cbpb.2005.04.016Scopus ID
2-s2.0-26644467234 (requires institutional sign-in at Scopus site) 63 CitationsAbstract
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.
Author List
Jeffers A, Xu X, Huang KT, Cho M, Hogg N, Patel RP, Kim-Shapiro DBAuthor
Neil Hogg PhD Senior Associate Dean, Professor in the Biophysics department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBiological Assay
Cell Line
Computer Simulation
Cyclic AMP
Cyclic GMP
Diffusion
Enzyme Activation
Erythrocytes
Guanylate Cyclase
Hemoglobins
Humans
Immunoenzyme Techniques
Insecta
Models, Biological
Models, Chemical
Nitric Oxide
Nitrites
Receptors, Cytoplasmic and Nuclear
Soluble Guanylyl Cyclase
Vasodilation
