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Research ArticleArticle

Role of an ATP-Sensitive Potassium Channel Opener, YM934, in Mitochondrial Energy Production in Ischemic/Reperfused Heart

Kouichi Tanonaka, Taku Taguchi, Miki Koshimizu, Tsuyoshi Ando, Tomohiro Morinaka, Tomoya Yogo, Fusako Konishi and Satoshi Takeo
Journal of Pharmacology and Experimental Therapeutics November 1999, 291 (2) 710-716;
Kouichi Tanonaka
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Taku Taguchi
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Miki Koshimizu
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Tsuyoshi Ando
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Tomohiro Morinaka
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Tomoya Yogo
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Fusako Konishi
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Satoshi Takeo
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Abstract

We examined a possible mechanism of action of an ATP-sensitive potassium (KATP) channel opener, YM934, for the improvement of energy metabolism in hearts subjected to 35-min ischemia and 60-min reperfusion. The treatment with 30 nM YM934 for the final 15 min of preischemia enhanced postischemic recovery of left ventricular developed pressure, attenuated the postischemic rise in left ventricular end-diastolic pressure, and suppressed the release of creatine kinase and ATP metabolites during reperfusion. The treatment also restored myocardial ATP and creatine phosphate contents and attenuated the decrease in mitochondrial oxygen consumption rate during reperfusion. The higher mitochondrial function was also seen in YM934-treated hearts at the end of ischemia. In another set of experiments, myocardial skinned bundles were incubated for 30 min under hypoxic conditions in the presence and absence of YM934, and then mitochondrial oxygen consumption rate was determined. Hypoxia decreased the mitochondrial oxygen consumption rate of skinned bundles to approximately 40% of the prehypoxic value. In contrast, the treatment of skinned bundles with 30 nM YM934 preserved the mitochondrial oxygen consumption rate during hypoxia. The effect of YM934 on the hypoxic skinned bundles was abolished by combined treatment with either the KATP channel blocker glyburide or the mitochondrial KATP channel blocker 5-hydroxydecanoate in a concentration-dependent manner. The results suggest that YM934 is capable of attenuating ischemia/reperfusion injury of isolated perfused hearts due to preservation of mitochondrial function during ischemia, probably through opening of mitochondrial KATP channels.

Footnotes

  • Send reprint requests to: Satoshi Takeo, Ph.D., Department of Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan. E-mail:takeos{at}ps.toyaku.ac.jp

  • Abbreviations:
    KATP
    ATP-sensitive potassium
    CK
    creatine kinase
    CP
    creatine phosphate
    5-HD
    5-hydroxydecanoate
    LVDP
    left ventricular developed pressure
    LVEDP
    left ventricular end-diastolic pressure
    • Received May 12, 1999.
    • Accepted July 23, 1999.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 291 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 291, Issue 2
1 Nov 1999
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Research ArticleArticle

Role of an ATP-Sensitive Potassium Channel Opener, YM934, in Mitochondrial Energy Production in Ischemic/Reperfused Heart

Kouichi Tanonaka, Taku Taguchi, Miki Koshimizu, Tsuyoshi Ando, Tomohiro Morinaka, Tomoya Yogo, Fusako Konishi and Satoshi Takeo
Journal of Pharmacology and Experimental Therapeutics November 1, 1999, 291 (2) 710-716;

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Research ArticleArticle

Role of an ATP-Sensitive Potassium Channel Opener, YM934, in Mitochondrial Energy Production in Ischemic/Reperfused Heart

Kouichi Tanonaka, Taku Taguchi, Miki Koshimizu, Tsuyoshi Ando, Tomohiro Morinaka, Tomoya Yogo, Fusako Konishi and Satoshi Takeo
Journal of Pharmacology and Experimental Therapeutics November 1, 1999, 291 (2) 710-716;
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