Ryanodine prolongs Ca‐currents while suppressing contraction in rat ventricular muscle cells

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Abstract
Ryanodine (1 μm) suppressed or abolished contraction in response to step depolarizations in voltage‐clamped cells isolated from adult rat ventricular myocardium. The step depolarizations evoked the second inward current, which is carried largely by Ca ions under these conditions, and there was little or no change in the amplitude of this current when contraction was reduced or abolished by ryanodine. The effects of ryanodine on contraction were, however, accompanied by a prolongation of the second inward current resulting from a slowing of the apparent inactivation of this current. It is suggested that ryanodine affects steps in excitation‐contraction coupling subsequent to the second inward current, perhaps Ca‐release from intracellular stores, and that this slows a Ca‐dependent inactivation of second inward current.