Mitochondrial nitric oxide inhibits ATP synthesis effect of free calcium in rat heart

Alfredo Saavedra-Molina, J. Ramírez-Emiliano, M. Clemente-Guerrero, V. Pérez-Vázquez, L. Aguilera-Aguirre, J. C. González-Hernández

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


Nitric oxide is a small potentially toxic molecule and a diatomic free radical. We report the interaction of L-arginine, oxygen and calcium with the synthesis of nitric oxide in heart mitochondria. Nitric oxide synthesis is increased in broken rat heart mitochondria compared with intact and permeabilized mitochondria. Intact mitochondria subjected to hypoxia-reoxygenation conditions accumulated nitric oxide that inhibits oxygen consumption and ATP synthesis. ATPase activity is not affected during this augment of nitric oxide. Physiological free calcium concentrations protected mitochondria from the damage caused by the accumulation of nitric oxide. Higher concentrations of the divalent cation increase the damage exerted by nitric oxide.

Original languageEnglish (US)
Pages (from-to)95-102
Number of pages8
JournalAmino Acids
Issue number1-2
StatePublished - Mar 2003
Externally publishedYes


  • ATP synthesis
  • Calcium
  • Heart
  • Hypoxia-reoxygenation
  • Mitochondria
  • Nitric oxide

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Organic Chemistry


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