doi: 10.1161/01.RES.0000126697.64381.37
© 2004 American Heart Association, Inc.
Editorials |
NO Contest
Nitrite Versus S-Nitroso-Hemoglobin
From the Critical Care Medicine Department (M.T.G.), Warren G. Magnuson Clinical Center, National Institutes of Health; Cardiovascular Branch (M.T.G.), National Heart, Lung, and Blood Institute, National Institutes of Health; Laboratory of Chemical Biology (M.T.G., A.N.S.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Md.
Correspondence to Mark Gladwin, Critical Care Medicine Department, CC, Laboratory of Chemical Biology, NIDDK, National Institutes of Health, Building 10/7D43, 10 Center Dr, Bethesda, MD 20892-1662. E-mail mgladwin@cc.nih.gov
See related article, pages 976–983
Key Words: nitric oxide • S-nitroso-hemoglobin • hemoglobin • iron-nitrosyl-hemoglobin • nitrite
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
A recent flurry of research papers and commentaries in this journal1–4 has highlighted a current major controversy in cardiovascular biochemistry and physiology: how is nitric oxide (NO) transported in the bloodstream. Two views have arisen. First, that S-nitrosated hemoglobin and albumin serve as stable storage forms of intravascular NO, and, in the case of S-nitrosated hemoglobin, as an allosterically regulated delivery vehicle for NO.5,6 The second is that the anion nitrite, which is present in relative abundance in both blood and tissue, subserves this function.7
The controversy is relevant to the study by James et al in this issue of Circulation Research that examined the ability of red blood cells treated with NO, from healthy subjects and patients with diabetes, to vasodilate rabbit aortic rings.4 The investigators report that exposure of oxygenated red blood cells to NO in vitro results in increased levels of NO-modified hemoglobin, specifically iron-nitrosyl-hemoglobin (NO bound to the heme group) and S-nitroso-hemoglobin (NO bound to the cysteine 93 residue of the ß-globin chain), and that these cells vasodilate rabbit aortic rings. The ability of the NO-treated red blood cells to vasodilate increases with greater NO exposure, raising intracellular S-nitroso-hemoglobin levels and with progressive hypoxia. Additionally, they find that diabetic red blood cells form less S-nitroso-hemoglobin with NO exposure than normal red blood cells, dilate more at 1% oxygen concentration, and dilate less at 2% oxygen. They ascribe these observations to an impairment in NO delivery from glycohemoglobin (at 2% oxygen) and suggest that
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