Implication of Mitochondrial NO/cGMP/PKG Signaling System in the Activation and Inhibition of Mitochondrial Respiration by L-Arginine and NO Donors

The results suggest that the functioning of calcium-dependent mitochondrial calcium-dependent NO synthase /GC/protein kinase G -SS can ensure the activation of respiration at low concentrations of L-arginine or sodium nitroprusside in the medium

V. V. Dynnik; E. V. Grishina; N. I. Fedotcheva

2020

Scholarcy highlights

  • The involvement of the mitochondrial calcium-dependent NO synthase in the regulation of mitochondrial respiration has not been sufficiently studied
  • The high rate of mitochondrial respiration was supported by pyruvate and glutamate or by succinate in the presence of hexokinase, glucose, and ADP
  • It was shown that L-arginine and the NO donor sodium nitroprusside exert concentration-dependent effects on the mitochondrial respiration rate
  • The inhibitors of NOS, GC, and protein kinase G eliminated this effect indicating that mitochondrial calcium-dependent NO synthase/GC/PKG-SS is involved in the activation of respiration
  • The inhibitors of GC and PKG enhanced the inhibition of respiration, which indicates an opposite effect of the excess of NO and PKG on the mitochondrial respiration
  • The results suggest that the functioning of calcium-dependent mtNOS/GC/PKG-SS can ensure the activation of respiration at low concentrations of L-arginine or SNP in the medium
  • The results suggest that the functioning of calcium-dependent mitochondrial calcium-dependent NO synthase/GC/protein kinase G-SS can ensure the activation of respiration at low concentrations of L-arginine or sodium nitroprusside in the medium

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