Calcium current in isolated neonatal rat ventricular myocytes.

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Abstract
1. Calcium currents (ICa) from neontal rat ventricular heart muscle cells grown in primary culture were examined using the ''whole-cell'' voltage-clamp technique (Hamill, Marty, Neher, Sakmann and Sigworth, 1981). Examination of ICa was limited to one calcium channel type, ''L'' type (Nilius, Hess, Lansman and Tsien, 1985), by appropriate voltage protocols. 2. We measured transient and steady-state components of ICa, and could generally describe ICa in terms of the steady-state activation (d.infin.) and inactivation (f.infin.) meters. 3. We observed that the reduction of ICa by the calcium channel antagonist D600 can be explained by both a shift of d.infin. to more positive potentials as well as a slight reduction of ICa conductance. D600 did not significantly alter either the rate of inactivation of ICa or the voltage dependence of f.infin.. 4. The calcium channel modulator BAY K8644 shifted both d.infin. and f.infin. to more negative potentials. Additionally, BAY K8644 increased the rate of inactivaiton at potentials between +5 and +55 mV. Furthermore, BAY K8644 also increased ICa conductance, a change consistent with a promotion of ''mode 2'' calcium channel activity (Hess, Lansman and Tsien, 1984). 5. We conclude that, as predicted by d.infin. and f.infin. there is a significant steady-state component of ICa (''window current'') at plateau potnetials in neonatal rat heart cells. Modulation of the steady-state and transient components of ICa by various agents can be attributed both to specific alterations in d.infin. and f.infin. and to more complicated alterations in the mode of calcium channel activity.