TY - JOUR
T1 - Tetrodotoxin-blockable calcium currents in rat ventricular myocytes; A third type of cardiac cell sodium current
AU - Aggarwal, R.
AU - Shorofsky, S. R.
AU - Goldman, L.
AU - Balke, C. W.
PY - 1997/12/1
Y1 - 1997/12/1
N2 - 1. Whole-cell patch clamp currents from freshly isolated adult rat ventricular cells, recorded in external Ca2+ (Ca(o)2+) but no external Na+ (Na(o)+), displayed two inward current components: a smaller component that activated over more negative potentials and a larger component (L-type Ca2+ current) that activated at more positive potentials. The smaller component was not generated by Ca2+ channels. It was insensitive to 50 μM Ni2+ and 10 μM La3+, but suppressed by 10 μM tetrodotoxin (TTX). We refer to this component as I(Ca(TTX)). 2. The conductance-voltage, g(V), relation in Ca(o)2+ only was well described by a single Boltzmann function (half-maximum potential, V( 1/4 ), of -44.5; slope factor, k, of -4.49 mV, means of 3 cells). g(V) in Ca(o)2+ plus Na(o)+ was better described as the sum of two Boltzmann functions, one nearly identical to that in Ca(o)2+ only (mean V( 1/4 ) of -45.1 and k of -3.90 mV), and one clearly distinct (mean V( 1/4 ) of -35.6 and k of -2.31 mV). Mean maximum conductance for I(Ca(TTX)) channels increased 23.7% on adding 1 mM Na0+ to 3 mM Ca(o)2+. I(Ca(TTX)) channels are permeable to Na+ ions, insensitive to Ni2+ and La3+ and blocked by TTX. They are Na+ channels. 3. I(Ca(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.
AB - 1. Whole-cell patch clamp currents from freshly isolated adult rat ventricular cells, recorded in external Ca2+ (Ca(o)2+) but no external Na+ (Na(o)+), displayed two inward current components: a smaller component that activated over more negative potentials and a larger component (L-type Ca2+ current) that activated at more positive potentials. The smaller component was not generated by Ca2+ channels. It was insensitive to 50 μM Ni2+ and 10 μM La3+, but suppressed by 10 μM tetrodotoxin (TTX). We refer to this component as I(Ca(TTX)). 2. The conductance-voltage, g(V), relation in Ca(o)2+ only was well described by a single Boltzmann function (half-maximum potential, V( 1/4 ), of -44.5; slope factor, k, of -4.49 mV, means of 3 cells). g(V) in Ca(o)2+ plus Na(o)+ was better described as the sum of two Boltzmann functions, one nearly identical to that in Ca(o)2+ only (mean V( 1/4 ) of -45.1 and k of -3.90 mV), and one clearly distinct (mean V( 1/4 ) of -35.6 and k of -2.31 mV). Mean maximum conductance for I(Ca(TTX)) channels increased 23.7% on adding 1 mM Na0+ to 3 mM Ca(o)2+. I(Ca(TTX)) channels are permeable to Na+ ions, insensitive to Ni2+ and La3+ and blocked by TTX. They are Na+ channels. 3. I(Ca(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.
UR - http://www.scopus.com/inward/record.url?scp=0031464230&partnerID=8YFLogxK
U2 - 10.1111/j.1469-7793.1997.353bb.x
DO - 10.1111/j.1469-7793.1997.353bb.x
M3 - Article
C2 - 9423179
AN - SCOPUS:0031464230
VL - 505
SP - 353
EP - 369
JO - Journal of Physiology
JF - Journal of Physiology
SN - 0022-3751
IS - 2
ER -