Muscle contraction and inward current induced by silver and effect of Ca2+ channel blockers
Oba, T.; Aoki, T.; Koshita, M.; Nihonyanagi, K.; Yamaguchi, M.
American Journal of Physiology 264(4 Pt 1): C852-C856
1993
ISSN/ISBN: 0002-9513 PMID: 8386451 Document Number: 406465
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 mM Ag+. Exposure of fibers to Cd2+ completely inhibited tonic contraction and modified phasic contraction to some extent. Nifedipine at 10 mM initially potentiated and then completely inhibited twitch tension; subsequently, fibers no longer contracted phasically in response to 20 mM 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 mM 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 mM nifedipine, the inward current induced by 10 mM 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. Reprinted by permission of the publisher.