MUSCLE-CONTRACTION AND INWARD CURRENT INDUCED BY SILVER AND EFFECT OFCA2+ CHANNEL BLOCKERS

Single fibers from toe or anterior tibialis muscle contracted transien tly and then tonically in the presence of 1.8 mM Ca2+ on addition of 1 0 muM Ag+. Exposure of fibers to Cd2+ Completely inhibited tonic contr action and modified phasic contraction to some extent. Nifedipine at 1 0 muM initially potentiated and then completely inhibited twitch tensi on; subsequently, fibers no longer contracted phasically in response t o 20 muM Ag+, whereas slight tonic contraction still occurred. Fibers with membrane potential clamped at -90 mV produced maintained inward c urrent on application of Ag+. Simultaneous administration of 1 mM Cd2 and 10 muM Ag+ to fibers voltage clamped with the double mannitol gap technique almost completely blocked the inward current. Removal of Cd 2+ elicited a rapid and large inward current. Ag+-induced inward curre nt was inhibited when 1 mM Cd2+ was applied to fibers during developme nt of the inward current. In fibers paralyzed with 10 muM nifedipine, the inward current induced by 10 muM Ag+ was partially inhibited. Thes e results suggest that phasic contraction induced by Ag+ is controlled by L-type Ca2+ channels (probably voltage sensors) located in the T-t ubular membrane, whereas tonic contraction involves Ca2+ channels sens itive and/or insensitive to dihydropyridine in the surface and T-tubul ar membranes.