HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 293/3/H1508    most recent 01259.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (11) Citing Articles via Google Scholar Google Scholar Articles by Blood, A. B. Articles by Power, G. G. Search for Related Content PubMed PubMed Citation Articles by Blood, A. B. Articles by Power, G. G.

In vitro and in vivo kinetic handling of nitrite in blood: effects of varying hemoglobin oxygen saturation

¹Center for Perinatal Research and Division of Neonatology, ²Department of Pediatrics, Loma Linda University School of Medicine, Loma Linda, California

Submitted 17 November 2006 ; accepted in final form 16 May 2007

Growing evidence suggests that nitrite, acting via reduction to nitric oxide by deoxyhemoglobin, may play an important role in local control of blood flow during hypoxia. To investigate the effect of hypoxia (65 Torr arterial PO₂) on the kinetic properties of nitrite, a bolus injection of sodium nitrite (10 mg/kg iv) was given to normoxic or hypoxic newborn lambs, and the time course of plasma nitrite and methemoglobin (MetHb) concentrations was measured. The in vivo kinetics of nitrite disappearance from plasma were biphasic and were not affected by hypoxia. Changes in MetHb, a product of the nitrite-hemoglobin reaction, also did not differ with the level of oxygenation. Hypoxia potentiated the hypotensive effects of nitrite on pulmonary and systemic arterial pressures. The disappearance of nitrite from plasma was equivalent to the increase in MetHb on a molar basis. In contrast, nitrite metabolism in sheep blood in vitro resulted in more than one MetHb per nitrite equivalent under mid- and high-oxygenation conditions: oxyhemoglobin (HbO₂) saturation = 50.3 ± 1.7% and 97.0 ± 1.3%, respectively. Under the low-oxygenation condition (HbO₂ saturation = 5.2 ± 0.9%), significantly less than 1 mol of MetHb was produced per nitrite equivalent, indicating that a significant portion of nitrite is metabolized through pathways that do not produce MetHb. These data support the idea that the vasodilating effects of nitrite are potentiated under hypoxic conditions due to the reduction of nitrite to nitric oxide by deoxyhemoglobin.

methemoglobin; hypoxia; nitric oxide

This article has been cited by other articles:

				Z. Cao, J. B. Bell, J. G. Mohanty, E. Nagababu, and J. M. Rifkind Nitrite enhances RBC hypoxic ATP synthesis and the release of ATP into the vasculature: a new mechanism for nitrite-induced vasodilation Am J Physiol Heart Circ Physiol, October 1, 2009; 297(4): H1494 - H1503. [Abstract] [Full Text] [PDF]

				D. A. Vitturi, X. Teng, J. C. Toledo, S. Matalon, J. R. Lancaster Jr., and R. P. Patel Regulation of nitrite transport in red blood cells by hemoglobin oxygen fractional saturation Am J Physiol Heart Circ Physiol, May 1, 2009; 296(5): H1398 - H1407. [Abstract] [Full Text] [PDF]

				A. B. Blood, M. Tiso, S. T. Verma, J. Lo, M. S. Joshi, I. Azarov, L. D. Longo, M. T. Gladwin, D. B. Kim-Shapiro, and G. G. Power Increased nitrite reductase activity of fetal versus adult ovine hemoglobin Am J Physiol Heart Circ Physiol, February 1, 2009; 296(2): H237 - H246. [Abstract] [Full Text] [PDF]

				D. B. Casey, A. M. Badejo Jr., J. S. Dhaliwal, S. N. Murthy, A. L. Hyman, B. D. Nossaman, and P. J. Kadowitz Pulmonary vasodilator responses to sodium nitrite are mediated by an allopurinol-sensitive mechanism in the rat Am J Physiol Heart Circ Physiol, February 1, 2009; 296(2): H524 - H533. [Abstract] [Full Text] [PDF]