The aim of this paper was to estimate the Ca content of the sarcoplasmic reticulum (s.r.) and to compare this with the amount of Ca which enters the cell via the calcium current in systole. The s.r. Ca content was measured electrophysiologically in voltage-clamped rat ventricular myocytes. Rapid application of caffeine produced a transient increase of [Ca2+]i which was accompanied by a transient inward Na-Ca exchange current. The integral of this current gives a measure of the Ca2+ pumped out of the cell by Na-Ca exchange. Ni2+ (5 mM) inhibited the current and decreased the rate of fall of [Ca2+]i to 32% of the control suggesting that Na-Ca exchange is responsible for 68% of Ca removal from the cytoplasm following the addition of caffeine. Correcting for the Na-Ca independent Ca removal suggests that the s.r. Ca content is equivalent to about 120 mumol per litre cell. Furthermore we estimate that, during systole, Ca entry into the cell via the sarcolemmal calcium current is equal to about 6% of the Ca content of the s.r.

The effects of high (20 mm) concentrations of caffeine were studied on the transmembrane voltage and currents in rat single ventricular myocytes by the whole cell configuration of the patch clamp technique. Rapid application of caffeine released Ca2+ from the sarcoplasmic reticulum and induced a Ni2+‐sensitive transient inward current with concomitant change of the transmembrane voltage from −72.6 ± 0.4 to −68.0 ± 0.6 mV (n = 4). Maintained application of caffeine lengthened the action potential duration (APD90) from 66.7 ± 16.9 to 135.1 ± 34.1 ms (n = 4) and depressed the amplitude of both the inward rectifier potassium and the inward calcium currents. It is concluded that these effects of caffeine should be recognized when it is used as a tool to study electromechnical coupling.

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