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Novel isoform of Ca2+ channel in rat fetal cardiomyocytes.
Author(s) -
Tohse N,
Masuda H,
Sperelakis N
Publication year - 1992
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1992.sp019165
Subject(s) - nifedipine , nitrendipine , dihydropyridine , chemistry , antagonist , patch clamp , medicine , depolarization , diltiazem , channel blocker , membrane potential , isradipine , biophysics , voltage dependent calcium channel , endocrinology , electrophysiology , calcium , receptor , biology , biochemistry
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.