Novel isoform of Ca2+ channel in rat fetal cardiomyocytes.

Abstract

1. 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. © 1992 The Physiological Society