AJP - Cell Physiology, Vol 264, Issue 4 C852-C856, Copyright © 1993 by American Physiological Society
Muscle contraction and inward current induced by silver and effect of Ca2+ channel blockers
T. Oba, T. Aoki, M. Koshita, K. Nihonyanagi and M. Yamaguchi
Department of Physiology, Nagoya City University Medical School, Japan.
Single fibers from toe or anterior tibialis muscle contracted transiently
and then tonically in the presence of 1.8 mM Ca2+ on addition of 10 microM
Ag+. Exposure of fibers to Cd2+ completely inhibited tonic contraction and
modified phasic contraction to some extent. Nifedipine at 10 microM
initially potentiated and then completely inhibited twitch tension;
subsequently, fibers no longer contracted phasically in response to 20
microM Ag+, whereas slight tonic contraction still occurred. Fibers with
membrane potential clamped at -90 mV produced maintained inward current on
application of Ag+. Simultaneous administration of 1 mM Cd2+ and 10 microM
Ag+ to fibers voltage clamped with the double mannitol gap technique almost
completely blocked the inward current. Removal of Cd2+ elicited a rapid and
large inward current. Ag(+)-induced inward current was inhibited when 1 mM
Cd2+ was applied to fibers during development of the inward current. In
fibers paralyzed with 10 microM nifedipine, the inward current induced by
10 microM Ag+ was partially inhibited. These results suggest that phasic
contraction induced by Ag+ is controlled by L-type Ca2+ channels (probably
voltage sensors) located in the T-tubular membrane, whereas tonic
contraction involves Ca2+ channels sensitive and/or insensitive to
dihydropyridine in the surface and T-tubular membranes.
