The model of calcium-channel gating described above, although almost certainly too simple, suggests a direct role for protein kinases and phosphatases in determining the kinetics of calcium channel gating on a subsecond time scale. In addition, it provides a unique perspective for understanding studies of calcium channel gating under widely different metabolic and pharmacological conditions. Although many of these effects may be specific to the dihydropyridine-sensitive or L-type calcium channel, they give an indication of the range of possibilities for integrating calcium-channel activity with cellular biochemistry.