Physiological modulation of inactivation in L-type Ca2+ channels: one switch.

@article{Findlay2004PhysiologicalMO,
  title={Physiological modulation of inactivation in L-type Ca2+ channels: one switch.},
  author={Ian Findlay},
  journal={The Journal of physiology},
  year={2004},
  volume={554 Pt 2},
  pages={275-83}
}
The relative contributions of voltage- and Ca(2+)-dependent mechanisms of inactivation to the decay of L-type Ca(2+) channel currents (I(CaL)) is an old story to which recent results have given an unexpected twist. In cardiac myocytes voltage-dependent inactivation (VDI) was thought to be slow and Ca(2+)-dependent inactivation (CDI) resulting from Ca(2+) influx and Ca(2+)-induced Ca(2+)-release (CICR) from the sarcoplasmic reticulum provided an automatic negative feedback mechanism to limit Ca… CONTINUE READING

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In cardiac myocytes voltage - dependent inactivation ( VDI ) was thought to be slow and Ca(2+)-dependent inactivation ( CDI ) resulting from Ca(2 + ) influx and Ca(2+)-induced Ca(2+)-release ( CICR ) from the sarcoplasmic reticulum provided an automatic negative feedback mechanism to limit Ca(2 + ) entry and the contribution of I(CaL ) to the cardiac action potential .
In cardiac myocytes voltage - dependent inactivation ( VDI ) was thought to be slow and Ca(2+)-dependent inactivation ( CDI ) resulting from Ca(2 + ) influx and Ca(2+)-induced Ca(2+)-release ( CICR ) from the sarcoplasmic reticulum provided an automatic negative feedback mechanism to limit Ca(2 + ) entry and the contribution of I(CaL ) to the cardiac action potential .
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