The transduction of action potential to muscle contraction (E–C coupling) is an example of fast communication between plasma membrane events and the release of calcium from an internal store, which in muscle is the sarcoplasmic reticulum (SR)¹. One theory is that the release channels of the SR are controlled by voltage-sensing molecules or complexes, located in the transverse tubular (T)-membrane, which produce, as membrane voltage varies, 'intramembrane charge movements'², but nothing is known about the structure of such sensors. Receptors of the Ca-channel-blocking dihydropyridines present in many tissues³, are most abundant in T-tubular muscle fractions^4,5 from which they can be isolated as proteins. Fewer than 5% of muscle dihydropyridines are functional Ca channels⁶; there is no known role for the remainder in skeletal muscle physiology. We report here that low concentrations of a dihydropyridine inhibit charge movements and SR calcium release in parallel. The effect has a dependence on membrane voltage analogous to that of specific binding of dihydropyridines⁶. We propose specifically that the molecule that generates charge movement is the dihydropyridine receptor.