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Tetrodotoxin‐blockable calcium currents in rat ventricular myocytes; a third type of cardiac cell sodium current
Author(s) -
Aggarwal R.,
Shorofsky S. R.,
Goldman L.,
Balke C. W.
Publication year - 1997
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 - 10.1111/j.1469-7793.1997.353bb.x
Subject(s) - tetrodotoxin , chemistry , conductance , sodium , biophysics , calcium , patch clamp , sodium channel , myocyte , endocrinology , physics , biochemistry , biology , receptor , organic chemistry , condensed matter physics
1 Whole‐cell patch clamp currents from freshly isolated adult rat ventricular cells, recorded in external Ca 2+ (Ca 2+ o ) but no external Na + (Ma 4 o ), displayed two inward current components: a smaller component that activated over more negative potentials and a larger component (L‐type Ca 2+ current) that activated at more positive potentials. The smaller component was not generated by Ca 2+ channels. It was insensitive to 50 μ m M 2+ and 10 μ m La 3+ , but suppressed by 10 μ m tetrodotoxin (TTX). We refer to this component as I Ca(TTx) . 2 The conductance–voltage, g(V) , relation in Ca 2+ o only was well described by a single Boltzmann function (half‐maximum potential, V ½ , of –44.5; slope factor, k , of –4.49 mV, means of 3 cells). g(V) in Ca 2+ o plus Na 4 o was better described as the sum of two Boltzmann functions, one nearly identical to that in Ca 2+ o only (mean V ½ of –45.1 and k of – 3.90 mV), and one clearly distinct (mean V ½ of –35.6 and k of –2.31 mV). Mean maximum conductance for I Ca(TTX) channels increased 23.7 % on adding 1 m m Na + o to 3 m m Ca 2+ o . I Ca(TTx) channels are permeable to Na + ions, insensitive to Ni 2+ and La 3+ and blocked by TTX. They are Na + channels. 3 ICa(TTx) channels are distinct from classical cardiac Na + channels. They activate and inactivate over a more negative range of potentials and have a slower time constant of inactivation than the classical Na + channels. They are also distinct from yet another rat ventricular Na + current component characterized by a much higher TTX sensitivity and by a persistent, non‐fast‐inactivating fraction. That I Ca(TTx) channels activate over a more negative range of potentials than classical cardiac Na + channels suggests that they may be critical for triggering the ventricular action potential and so of importance for cardiac arrhythmias.