Submaximal sodium-lack contractures in rapidly perfused frog ventricular strips.

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Rapid perfusion of strips of frog ventricular muscle (width less than or equal to 8 mm) by sodium-free Ringer yielded contractures with very fast rates of rise (half time approximately equal to 2 s) and flat plateaus. Tension in lithium Ringer was 0.64 (0.38-0.77) of the maximal tension the muscle could produce [i.e., for an extracellular potassium concentration ([K]o) of 160 mM, and an [Na]o of 0 mM at less than 15 degrees C], showing that intracellular calcium concentration ([Ca]i) in zero [Na]o and normal [K]o was insufficient to saturate the myofilaments. Tension was related to [Ca]o in an S-shaped manner (apparent Km = 1.3 microM), was rapidly increased by electrical depolarization, high potassium, or low temperature, but was unaffected by up to 10(-5) M dihydroouabain. From these data was derived the working hypothesis that the value of [Ca]i during the contracture plateau is a steady-state value due to influx through a sodium-dependent mechanism and calcium uptake or efflux via a sodium-independent mechanism. Also, 1 microM dihydroouabain increased peak twitch tension by 60% but did not potentiate tension during the plateaus of contractures obtained by partial replacement of Nao. This result supports the working hypothesis and suggests that the potentiating effect of raising Nai may depend on the membrane potential (D. A. Eisner, W. J. Ledener, and R. D. Vaughan-Jones. J. Physiol. Lond. 335: 723-743, 1983).