A slow inward current is often reported in the range of -40 mV in ventricular myocytes in the presence of low (or no) extracellular Na+ and normal extracellular Ca2+ and is variably attributed to ‘slip-mode conductance (SMC)’ of the phosphorylated Na+ channels and to a subtype of TTX-sensitive Ca2+ channel [INa(null) or ICa(TTX)] (1,2). It is also reported that ICa(TTX) is expressed specifically in the ventricular mycoytes away from the region of chronic infract and not in those from normal heart (3) or that it may be due to L-type Ca2+ current overlapping Na+ current (4). The present study was carried out on isolated rat left ventricular myocytes (rLVM) obtained from the myocardium away from the infarct and on Xenopus oocytes expressing hNaV1.5 to assess, (i) the status of ICa(TTX) in rLVM, and (ii) whether SMC contributes to ICa(TTX). The ventricular myocytes were isolated from the normal (n=10), sham (n=14), and infarcted (n=19) rat heart by collagenase dispersion technique (5). Whole-cell patch-clamp experiments on rLVM from all the three groups showed an inward current at depolarizing steps of -40 mV from h.p. of -80 mV or -130 mV in the presence of 0[Na]o and 1 mM [Ca]o, or 5 mM [Na]o and 1 mM [Ca]o. TTX (≥10 µM) added to the bathing solution blocked this inward current. Two electrode voltage clamp experiments on Xenopus oocytes expressing hNaV1.5 (n=9), with or without beta1 subunit, did not show any inward current in the range of -60 mV to +40 mV when bathed with 0[Na]o and 0.1-65 mM [Ca]o containing solution. Injection of Sp-cAMP, an activator of PKA, into the oocytes expressing hNaV1.5 also did not facilitate Ca2+ inward current through these channels. These observations indicate that ICa(TTX) is present in rLVM from both the normal heart and the heart with chronic infarction but is not observable in Xenopus oocytes expressing hNaV1.5.