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(Circulation Research. 1998;83:1067-1068.)
© 1998 American Heart Association, Inc.

Editorial

Nitric Oxide, Myocardial Oxygen Consumption, and ATP Synthesis

Joanne S. Ingwall, , Ralph A. Kelly

From the Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, Mass.

Correspondence to Joanne S. Ingwall, PhD, NMR Laboratory, Brigham and Women's Hospital, 221 Longwood Ave, Room 247, Boston, MA 02115. E-mail ingwall@bustoff.bwh.harvard.edu

Key Words: nitric oxide • oxygen consumption • ATP synthesis • heart • metabolic substrate

NO is a free radical gas, NO, in equilibrium with the closely related redox forms NO^- and NO⁺. With a molecular weight of only 30 Da/mol (for reference, molecular oxygen is 32 Da/mol), NO is readily diffusible. The half-life of NO is 0.1 to 5 seconds. NO synthesis is catalyzed by a family of proteins, NO synthases (NOSs). The NOS originally described as the source of NO in conduit vessel endothelial cells (eNOS or NOS3) has been found in the endothelium of the endocardium and the coronary vasculature, in atrial and ventricular myocytes, and in conduction cells of the heart.^{1 2 3}

Because NO is readily diffusible, it can affect many molecular targets. Molecular oxygen is itself a target, forming NO₂, which in turn forms NO₂^-_, and NO₃^-. NO reacts with the free radical superoxide O₂^- to form the highly reactive species peroxynitrite ONOO^-. NO also reacts with iron to form Fe²⁺NO complexes and with amino, thiol, diazo, and tyrosyl groups in proteins. On the basis of this chemistry, the macromolecular targets of NO and its derivatives in cells can be understood. For example, activation of the signal transduction protein guanylyl cyclase occurs via NO binding to its heme. Inhibition of creatine kinase and some of the glycolytic proteins, including GAPDH, by NO occurs by binding to labile reactive -SH groups. Thus, NO functions to alter macromolecular function in 2 distinct ways: by direct chemical modification and by activation of the guanylyl cyclase signaling pathway.

NO and ATP Synthesis

NO . . . [Full Text of this Article]

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