title: 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.
authors.affiliation: Department of Physiology and Biophysics, College of Medicine, University of Cincinnati, OH 45267.
authors.forename: N
authors.initials: N
authors.lastname: Tohse
authors.forename: H
authors.initials: H
authors.lastname: Masuda
authors.forename: N
authors.initials: N
authors.lastname: Sperelakis
mesh_terms: D000818:Animals; D002121:Calcium Channel Blockers / Q000145:classification / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D004594:Electrophysiology; D005318:Fetal Heart / Q000378:metabolism*; D066298:In Vitro Techniques; D007700:Kinetics; D009543:Nifedipine / Q000494:pharmacology; D051381:Rats
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D009543:Nifedipine