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) 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 (5) Citing Articles via Google Scholar Google Scholar Articles by Kreutzer, U. Articles by Jue, T. Search for Related Content PubMed PubMed Citation Articles by Kreutzer, U. Articles by Jue, T.

Role of myoglobin as a scavenger of cellular NO in myocardium

Department of Biological Chemistry, University of California Davis, Davis, California 95616

Submitted 4 February 2003 ; accepted in final form 20 October 2003

Recent studies have detected a ¹H nuclear magnetic resonance (NMR) reporter signal of metmyoglobin (metMb) during bradykinin stimulation of an isolated mouse heart. The observation has led to the hypothesis that Mb reacts with cellular nitric oxide (NO). However, the hypothesis depends on an unequivocal detection of metMb signals in vivo. In solution, nitrite oxidization of Mb produces a characteristic set of paramagnetically shifted ¹H NMR signals. In the upfield spectral region, MbO₂ and MbCO exhibit the CH₃ Val E11 signals at –2.8 and –2.4 ppm, respectively. In the same spectral region, nitrite oxidation of Mb produces a set of signals at –3.7 and –4.7 ppm at 35°C. Previous studies have confirmed the visibility of metMb signals in perfused rat myocardium. With bradykinin infusion, perfusion pressure and rate-pressure product decrease, consistent with endogenous NO formation. However, neither myocardial O₂ consumption nor high-energy phosphate levels, as reflected in the ³¹P NMR signals, show any significant change. Bradykinin still triggers a similar physiological response even in the presence of CO that is sufficient to inhibit 86% Mb. In all cases, the ¹H NMR spectra from perfused rat myocardium reveal no metMb signals. The results suggest that bradykinin-induced NO does not interact significantly with cellular Mb to produce an NMR-detectable quantity of metMb in the perfused rat myocardium. As a consequence, the experiments cannot confirm the intriguing proposal that Mb acts as a cellular NO scavenger.

nuclear magnetic resonance; heart; oxidative phosphorylation; bioenergetics; respiration

This article has been cited by other articles:

				S. Hazarika, M. Angelo, Y. Li, A. J. Aldrich, S. I. Odronic, Z. Yan, J. S. Stamler, and B. H. Annex Myocyte Specific Overexpression of Myoglobin Impairs Angiogenesis After Hind-Limb Ischemia Arterioscler Thromb Vasc Biol, December 1, 2008; 28(12): 2144 - 2150. [Abstract] [Full Text] [PDF]

				P.-C. Lin, U. Kreutzer, and T. Jue Myoglobin translational diffusion in rat myocardium and its implication on intracellular oxygen transport J. Physiol., January 15, 2007; 578(2): 595 - 603. [Abstract] [Full Text] [PDF]