Artículo de revista
Intracellular Ca2+ transients induced by high external K+ and tetracaine in cultured rat myotubes
Fecha
1994Registro en:
Cell Calcium (1994) 15, 356-368
01434160
10.1016/0143-4160(94)90011-6
Autor
Jaimovich Pérez, Enrique
Rojas, E.
Institución
Resumen
Cultured myotubes from rat neonatal skeletal muscle were used to measure
intracellular Ca2+ concentration ([Ca2ri) and membrane potentials (Vm) uslng the Indo-l
mlcrofluorimetry method and the nystatin perforated membrane patch technique, respectively.
Sudden increases in external [K$ from 5 mM to either 22, 42 or 34 mM elicited
transient elevations in [Ca2Q from a resting level of i03.2 ? 10.3 nM (n = 41) to peak values
of 297, 409 and 454 nM, respectively. Vm changes Induced by elevated [K$ followed the
Nernst equation for [Kyo. The complex Ca2+ release response induced by elevated [K$,
can be described by a minimal model involvin
9+
two components with different kinetics.
This analysis revealed that the extent of the Ca release by the fast component bears a
sigmoidal relationship with Vm (midpoint at -47.5 mV and an effective valence of 4). Furthermore,
while the fast transitory component was rather insensitive to [Ca2’10 and nifedipine,
the slow cotnponent was profoundly inhibited by the dihydropyridine (10 fl) both in
normal and in a Ca deficient medium. Tetracaine (0.05 to 2 mM), a blocker of the charge
movement associated with excitation-contraction (E-C) coupling, elicited a fast elevation in
[Ca2’]i followed by a rise at a constant rate to levels as high as 1-2 w, and the changes in
[Ca2’]i were readily reversible. Simultaneous measurements of Vm and [Ca2+]i suggest that
the fast component is coupled to the rapid depolarization of the membrane induced by the
anesthetic. We concluded that tetracaine triggers the release of Ca2+ from internal stores
by at least two different mechanisms, one of which Is associated with the depolarizing
effects of the drug.