EXTRACELLULAR CALCIUM-ION DEPLETION IN FROG CARDIAC VENTRICULAR MUSCLE

The extracellular free [Ca2+] in frog ventricular muscle strips was monitored using single-barrel Ca2+-selective microelectrodes. During trains of repetitive sitmulation, a heart rate-dependent, sustained fall (depletion) of the extracellular free [Ca2+] occurred, which was most likely a consequence of net Ca2+ influx into ventricular cells. The magnitude of the [Ca2+]o depletion increased for higher Ringer''s solution [Ca2+] and was reversibly blocked by Mn2+ ion. Prolonged repetitive field stimulation (20-30 min) activated additional cellular Ca2+ efflux, which can balance the additional Ca2+ influx caused by stimulation, resulting in abolition of extratrabecular [Ca2+]o depletion in 20-30 min, and hence 0 net transmembrane Ca2+ flux at steady state. In the poststimulation period of quiescence, cellular Ca2+ efflux persisted and caused an elevation (accumulation) of the extracellular free [Ca2+]. From these [Ca2+]o depletions, quantitative estimates for the net transmembrane Ca2+ flux were derived using an analytical solution to the diffusion equation. In the highest Ringer''s solution [Ca2+] used (1 mM) the calculated net increase of the total intracellular Ca per beat was 6.5 .+-. 1.4 .mu.mol/l of intracellular space. This corresponded to an average net transmembrane Ca2+ influx of 0.81 .+-. 0.17 pmol/cm2 per s during the 800-ms action potential. In lower bath [Ca2+] the net transmembrane [Ca2+] flux was proportionately reduced.