Abstract
The voltage sensing machinery of the skeletal muscle L-type CaV channel (CaV1.1) controls Ryanodine receptor (RyR1) activation, conferring voltage-dependence to the sarcoplasmic reticulum Ca2+ release channel. CaV1.1 channels possess four homologous but non-identical Voltage-Sensing Domains (VSDs), which undergo voltage-dependent rearrangements governing muscle contraction. CaV1 channels are the target of dihydropyridine drug family and, in skeletal muscle, nifedipine (a dihydropyridine antagonist) has been shown to inhibit CaV1.1 charge movement and sarcoplasmic reticulum Ca2+ release (Ríos and Brum, Nature 1987).
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