Excessive ATP hydrolysis in ischemic myocardium by mitochondrial F1F0-ATPase: effect of selective pharmacological inhibition of mitochondrial ATPase hydrolase activity.

@article{Grover2004ExcessiveAH,
  title={Excessive ATP hydrolysis in ischemic myocardium by mitochondrial F1F0-ATPase: effect of selective pharmacological inhibition of mitochondrial ATPase hydrolase activity.},
  author={G. Grover and K. Atwal and P. Sleph and Feng-li Wang and H. Monshizadegan and T. Monticello and D. Green},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2004},
  volume={287 4},
  pages={
          H1747-55
        }
}
  • G. Grover, K. Atwal, +4 authors D. Green
  • Published 2004
  • Biology, Medicine
  • American journal of physiology. Heart and circulatory physiology
  • Mitochondrial F(1)F(0)-ATPase normally synthesizes ATP in the heart, but under ischemic conditions this enzyme paradoxically causes ATP hydrolysis. Nonselective inhibitors of this enzyme (aurovertin, oligomycin) inhibit ATP synthesis in normal tissue but also inhibit ATP hydrolysis in ischemic myocardium. We characterized the profile of aurovertin and oligomycin in ischemic and nonischemic rat myocardium and compared this with the profile of BMS-199264, which only inhibits F(1)F(0)-ATP… CONTINUE READING
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