Evaluation of Nitric Oxide Formation from Nitrates in Pig Coronary Arteries.

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  • Aniya Yoko
    Laboratory of Physiology and Pharmacology, School of Health Sciences, School of Medicine, Faculty of Medicine, University of the Ryukyus Research Center of Comprehensive Medicine, School of Medicine, Faculty of Medicine, University of the Ryukyus
  • Uehara Naoko
    Laboratory of Physiology and Pharmacology, School of Health Sciences, School of Medicine, Faculty of Medicine, University of the Ryukyus
  • Ishii Chiho
    Laboratory of Physiology and Pharmacology, School of Health Sciences, School of Medicine, Faculty of Medicine, University of the Ryukyus
  • Suenaga Tuyoshi
    Laboratory of Physiology and Pharmacology, School of Health Sciences, School of Medicine, Faculty of Medicine, University of the Ryukyus
  • Wada Naomi
    Laboratory of Physiology and Pharmacology, School of Health Sciences, School of Medicine, Faculty of Medicine, University of the Ryukyus
  • Matsuzaki Toshihiro
    Department of Pharmacology, School of Medicine, Faculty of Medicine, University of the Ryukyus
  • Sakanashi Matao
    Research Center of Comprehensive Medicine, School of Medicine, Faculty of Medicine, University of the Ryukyus Department of Pharmacology, School of Medicine, Faculty of Medicine, University of the Ryukyus

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Abstract

To clarify the hypothesis that organic nitrates are converted to nitric oxide (NO) via nitrite ion (NO2-) by glutathione S-transferase, the metabolic conversion of four nitrates was examined in pig coronary arteries and compared with that in rat liver. Nitrates caused the relaxation of the artery muscles with the order of nitroglycerin > isosorbide dinitrate > nicorandil ≥ nipradilol, whereas the order of NO formation in the arteries was nitroglycerin > isosorbide dinitrate > nipradilol > nicorandil. The same order of NO formation from the nitrates was also observed in liver cytosol. Nicorandil may cause more relaxation than nipradilol by both NO releasing and other (unknown) actions. Although the order of the potency in N02 formation from the nitrates in liver cytosol was the same as that seen in NO formation, NO2- was not detected in pig coronary arteries. Thus NO2 formation from the nitrates correlated with NO formation in liver cytosol but not in pig arteries. When nonenzymatic and enzymatic NO formations from nitroglycerin were examined in the arteries, the enzymatic NO formation, which was not inhibited by glutathione S-transferase inhibitors, was 13% of the total NO. These results indicate that in pig coronary arteries, nitrates release NO mostly through a nonenzymatic manner, although there is a slight amount of enzymatically produced NO, and glutathione S-transferase may not contribute to the enzymatic NO formation.

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