Single cardiomyocytes of 18-day-old rat fetuses were isolated to characterize the cardiac Ca2+ channels in the fetal period, using whole-cell voltage clamp (Na+, K(+)-free external solution and K(+)-free internal solution), and depolarizing test pulses from a holding potential (HP) of -87 mV were applied. 2. The Ca2+ current was completely blocked by 2 mM-CO2+, but not completely blocked by the dihydropyridine (DHP) Ca2+ antagonist nifedipine. Nifedipine (3 microM) decreased the amplitude of the current (at -7 mV) by 65.9 +/- 3.4% (n = 20). At a HP of -47 mV, nifedipine decreased the Ca2+ current to about the same degree. Diltiazem (1 microM) did not block the nifedipine-resistant current which remained. 3. Nitrendipine, another DHP Ca2+ antagonist, had effects on the Ca2+ current similar to those of nifedipine. 4. The DHP-resistant current was not blocked by T-type channel blockers (Ni2+, tetramethrine) or an N-type blocker (omega-conotoxin). 5. In conclusion, rat fetal cardiomyocytes may have a unique type of Ca2+ channel (ICa(fe)), which decreases in amplitude and becomes less prominent during subsequent development.
