1. Twitch tension and intracellular Na+ activity (aiNa) were measured in voltage‐clamped sheep cardiac Purkinje fibres. aiNa was measured using Na+‐sensitive micro‐electrodes filled with the liquid ion exchange resin. ETH 227. The stimulus for contraction was a constant 200 ms depolarizing pulse to 0 mV from a holding potential of ‐80 mV delivered at 0.25 Hz. Prolonged test pulses for 1.8 s (post‐pulses) were applied at the end of the stimulus pulse. The effects of post‐pulses on twitch tension and aiNa were examined. 2. Post‐pulses in the range of ‐40 mV reduced twitch tension below control force produced without post‐pulse. Progressively more positive post‐pulses to levels above 0 mV profoundly increased twitch tension, with a greater than 400% rise in tension at +50 to +60 mV compared to control tension. aiNa declined at positive post‐pulse potentials by more than 2 mM at +30 to +40 mV. 3. Tetrodotoxin (100 microM) did not affect the post‐pulse voltage‐tension or voltage‐aiNa relation. Ca2+ channel modulation with nitrendipine (1 microM) similarly did not alter the post‐pulse voltage‐tension relation. 4. Removal of extracellular Na+ eliminated the nadir in tension at post‐pulses to ‐40 mV and the augmentation of tension at post‐pulses above 0 mV. 5. We interpret these findings as evidence of voltage‐sensitive Na‐Ca exchange promoting net Ca2+ influx and net Na+ efflux during positive post‐pulses. The unusual shape of the post‐pulse voltage‐tension relation curve can be accounted for by a charged‐carrier model of electrogenic Na‐Ca exchange. The inverse relation between aiNa and twitch tension probably reflects the combined effects of reduced aiNa leak and changes in Na+ and Ca2+ flux via voltage‐sensitive Na‐Ca exchange.
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