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Paired pulse stimulation increases the contractile strength of mammalian myocardium. If stimulation is discontinued the "potentiated state" takes several minutes to decay, as shown by the first contraction following resumption of stimulation. From earlier experiments it has been inferred that contractile force depends on Ca2+ released from intracellular stores rather than on an influx of Ca2+ associated with a given action potential. This view now receives support from the following findings: (1) Ni2+ and Co2+, known to inhibit Ca2+ influx during the action potential, when applied during a 2-minute rest period, are practically without effect on the strength of the first beat but strongly depress steady state contractions. (2) Caffeine, known to enhance Ca2+ efflux from and inhibit Ca2+ uptake into intracellular stores, greatly accelerates the decay of the potentiated state during a rest period. (3) Na+ -poor solution, known to inhibit Ca2+ efflux, has a strong positive inotropic effect. Paired pulse stimulation fails to increase contractile strength in Na+ -poor solution, and a rest period of many minutes is practically without effect on the amplitude of the first beat after resumption of stimulation. The results indicate that contraction is due to Ca2+ released from internal stores whose degree of filling can be altered.

The decay of the potentiated state in sheep and calf ventricular myocardial fibers. Influence of agents acting on transmembrane Ca2+ flux.