Effects of external Ca²⁺ concentration, Ca²⁺ channel blockers and chemical modification of SH groups in membrane proteins on silver ion (Ag⁺)-induced contraction were studied with single fibers of frog toe muscle. In the presence of 3mM Ca²⁺, Ag⁺ produced phasic (P₁) and subsequent tonic (P₂) contractions. When Ca²⁺ were replaced by Mg²⁺, only P₁ occurred upon Ag⁺. This type of contraction was completely blocked by 10μM nifedipine. P₂ was inhibited by application of 10μM nifedipine or 3mM Cd²⁺. When exposed to 1mM dithiothreitol (DTT) during contraction, the fiber rapidly decreased the tension to the resting level and then tension no longer developed. The fiber pretreated with 0.1% H₂O₂ for 10min did not respond upon 10μM Ag⁺. In such a fiber, reduction of SH groups by 10mM DTT for 2min restored the responsiveness of the fiber to Ag⁺. Ag⁺-induced contraction was not observed after exposure of the fiber to 20mM Hg²⁺ for 30min. These findings suggest that Ag⁺ has 2 sites to induce different types of contraction and that oxidation of SH groups in Ca²⁺ channels participates in Ag⁺-induced contraction.

Effects of external Ca²⁺ depletion and chemical modification of SH groups in membrane protein on gold-induced contraction were studied to compare with those by silver ion with single toe muscle fiber of frog. Membrane potential and twitch tension were also measured after exposure of fibers to gold ion. In Ringer solution, gold produced phasic (P₁) and subsequent tonic (P₂) contractions. When Ca²⁺ was replaced by Mg²⁺, only P₁ was elicited upon gold. Application of 5mM DTT to contracting fibers led to disappear the gold-induced tension rapidly and exponentially. The fiber pretreated with 0.05% H₂O₂ for 10min responded to occur no gold contraction. In such fibers paralyzed by H₂O₂, cleavage of SS bonds by DTT restored the responsiveness of fibers to gold ions. Gold ions depolarized the muscle membrane, dose-dependently. Twitch tension was first potentiated upon gold application, and then disappeared. These results indicate that action of gold ion on skeletal muscle is similar to that of Ag⁺, but the ability of chemical modification of sulfhydryls by gold ion in situ is much lesser than that by Ag⁺.