Calmodulin kinase II inhibition enhances ischemic preconditioning by augmenting ATP-sensitive K+ current.

@article{Li2007CalmodulinKI,
  title={Calmodulin kinase II inhibition enhances ischemic preconditioning by augmenting ATP-sensitive K+ current.},
  author={Jingdong Li and C{\'e}line Marionneau and Olha Koval and Leonid V. Zingman and Peter J. Mohler and Jeanne M Nerbonne and Mark E. Anderson},
  journal={Channels},
  year={2007},
  volume={1 5},
  pages={387-94}
}
Mice with genetic inhibition (AC3-I) of the multifunctional Ca(2+)/calmodulin dependent protein kinase II (CaMKII) have improved cardiomyocyte survival after ischemia. Some K(+) currents are up-regulated in AC3-I hearts, but it is unknown if CaMKII inhibition increases the ATP sensitive K(+) current (I(KATP)) that underlies ischemic preconditioning (IP) and confers resistance to ischemia. We hypothesized increased I(KATP) was part of the mechanism for improved ventricular myocyte survival… CONTINUE READING

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