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Am J Physiol Heart Circ Physiol 296: H237-H246, 2009. First published November 21, 2008; doi:10.1152/ajpheart.00601.2008
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Increased nitrite reductase activity of fetal versus adult ovine hemoglobin

Arlin B. Blood,1,2 Mauro Tiso,4 Shilpa T. Verma,3 Jennifer Lo,1 Mahesh S. Joshi,6 Ivan Azarov,6 Lawrence D. Longo,2 Mark T. Gladwin,4,5 Daniel B. Kim-Shapiro,6 and Gordon G. Power2

1Department of Pediatrics, Division of Neonatology, 2Center for Perinatal Biology, and 3Department of Anesthesiology, Loma Linda University School of Medicine, Loma Linda, California; 4Pulmonary and Vascular Medicine Branch, National Heart, Lung, and Blood Institute and 5Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, Maryland; and 6Department of Physics, Wake Forest University, Winston-Salem, North Carolina

Submitted 9 June 2008 ; accepted in final form 12 November 2008

Growing evidence indicates that nitrite, NO2–, serves as a circulating reservoir of nitric oxide (NO) bioactivity that is activated during physiological and pathological hypoxia. One of the intravascular mechanisms for nitrite conversion to NO is a chemical nitrite reductase activity of deoxyhemoglobin. The rate of NO production from this reaction is increased when hemoglobin is in the R conformation. Because the mammalian fetus exists in a low-oxygen environment compared with the adult and is exposed to episodes of severe ischemia during the normal birthing process, and because fetal hemoglobin assumes the R conformation more readily than adult hemoglobin, we hypothesized that nitrite reduction to NO may be enhanced in the fetal circulation. We found that the reaction was faster for fetal than maternal hemoglobin or blood and that the reactions were fastest at 50–80% oxygen saturation, consistent with an R-state catalysis that is predominant for fetal hemoglobin. Nitrite concentrations were similar in blood taken from chronically instrumented normoxic ewes and their fetuses but were elevated in response to chronic hypoxia. The findings suggest an augmented nitrite reductase activity of fetal hemoglobin and that the production of nitrite may participate in the regulation of vascular NO homeostasis in the fetus.

kinetics; nitric oxide; vascular control; fetus


Address for reprint requests and other correspondence: A. B. Blood, Dept. of Pediatrics, Div. of Neonatology, School of Medicine, Loma Linda Univ., Loma Linda, CA (e-mail: ablood{at}llu.edu)




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