Nitric oxide synthase in porcine heart mitochondria: Evidence for low physiological activity

Stephanie French, Cecilia R Giulivi, R. S. Balaban

Research output: Contribution to journalArticlepeer-review

80 Scopus citations


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·min-1) 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 protein-1·min-1) 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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number6 49-6
StatePublished - 2001
Externally publishedYes


  • ADP
  • ATP
  • Calcium
  • Oxidative phosphorylation
  • Oxygen consumption

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


Dive into the research topics of 'Nitric oxide synthase in porcine heart mitochondria: Evidence for low physiological activity'. Together they form a unique fingerprint.

Cite this