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1 Laboratory of Cardiac Energetics, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892; and 2 Department of Chemistry, University of Minnesota, Duluth, Minnesota 55812
The capacity of isolated porcine heart
mitochondria to produce nitric oxide (NO) via mitochondrial NO synthase
(NOS) was evaluated. The mitochondrial NOS content and activity (0.2 nmol NO · mg mitochondrial protein
1 · min1) were ~10 times
lower than previously reported for the rat liver. No evidence for
mitochondrial NOS-generated NO was found in mitochondrial suspensions
based on the lack of NO production and the lack of effect of either
L-arginine or NOS inhibitors on the rate of respiration. The reason that even the low mitochondrial NOS activity did not result
in net NO production and metabolic effects is because the mitochondrial
metabolic breakdown of NO (1-4 nmol NO · mg mitochondrial protein1 · min1) was greater than
the maximum rate of NO production measured in homogenates. These data
suggest that NO production at the mitochondria via NOS is not a
significant source of NO in the intact heart and does not regulate
cardiac oxidative phosphorylation.
oxidative phosphorylation; oxygen consumption; calcium; ATP; ADP
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