The aim of this paper was to characterize the pathways that allow Ca2+ ions to enter the cell at rest. Under control conditions depolarization produced an increase of intracellular Ca concentration ([Ca2+]i) that increased with depolarization up to about 0 mV and then declined. During prolonged depolarization the increase of [Ca2+]i decayed. This increase of [Ca2+]i was inhibited by nifedipine and the calculated rate of entry of Ca increased on depolarization and then declined with a similar timecourse to the inactivation of the L-type Ca current. We conclude that this component of change of [Ca2+ ]i is due to the L-type Ca current. If intracellular Na was elevated then only part of the change of [Ca2+]i was inhibited by nifedipine. The nifedipine-insensitive component increased monotonically with depolarization and showed no relaxation on prolonged depolarization. This component appears to result from Na-Ca exchange (NCX). When the L-type current and NCX were both inhibited (nifedipine and Na-free solution) then depolarization decreased and hyperpolarization increased [Ca2+]i. These changes of [Ca2+]i were unaffected by modifiers of B-type Ca channels such as chlorpromazine and AlF3 but were abolished by gadolinium ions. We conclude that, in addition to L-type Ca channels and NCX, there is another pathway for entry of Ca2+ into the ventricular myocyte but this is distinct from the previously reported B-type channel. © 2006 Elsevier Ltd. All rights reserved.