Tension development in frog skeletal muscle induced by silver ions.

Abstract

In single fibers of frog toe muscles placed in a Cl-free MOPS solution containing 1.8 mM Ca2+, tension developed slowly in the presence of very low concentrations of Ag+. This tension was not blocked by the administration of Co2+ or Nit +. On the other hand, two types of transient tensions developed with the application of 5 µM Ag+, in fibers pretreated with 0-Ca2+ MOPS solution, containing either 2 mM Co2+ or 1 mM Ni2+, for 10 min. In the presence of divalent cations or TTX, the first repetitive twitch-like contraction disappeared, indicating this tension is induced by action potentials repeatedly generated by the lack of divalent cations. The 2nd subsequent transient tension was caused by 5 uM Ag+ in the presence of various kinds of divalent cations, or TTX. After reversion to the resting tension, the fiber was contracted by adding more than 0.1 mM of Ca2+ or 25 mM caffeine to the external medium. Even when placed in a Ca2+-free solution containing 3 mM EGTA and 3 mM Mg2+ for 30 min, the fiber still developed an appreciable tension in response to 5 ~tM Ag+. These findings suggest that a transient development of the Ag+-induced tension does not require the presence of external Cat+. A specific sulfhydryl reagent, pCMPS, did not contract the muscle fiber. Therefore, Ag+ may develop tension by mediating unknown chemical reaction(s) other than the sulf hydryl group on T-tubular membrane proteins.

Modulation of the Ca2+ channel voltage sensor and excitation-contraction coupling by silver

“…Treatment of a frog skeletal muscle fiber with 10 ,uM Ag+ induced a transient contraction (Fig. 1 A) as previously reported by Oba and Hotta (7,8). Even after a subsequent wash with Ca> free nitrate Ringer and with Ringer (to remove Ag+), there was a complete inhibition of twitch, tetanus, and K+-induced tension.…”

“…These Ag+ contractions occur without membrane depolarization and in the presence of tetrodotoxin (8). They are abolished when the fiber is detubulated (by glycerine Ringer), suggesting a direct effect of Ag+ on E-C coupling at the level ofthe T-tubular system (7,8). Since the T-tubular Ca> channels are essential to E-C coupling, we examined the possibility that Ag+ interacts with the Ca" channel to produce contraction and the subsequent failure of E-C coupling.…”

“…Previously, Oba and Hotta have shown that Ag+ induces a transient contraction of intact skeletal muscle fibers followed by inhibition of E-C coupling (7). These Ag+ effects occur without membrane depolarization and require an intact T-tubule membrane system (7,8). In this paper we examine the effect of DHP calcium channel agonists and antagonists on Ag+ contractions and determine the effects of Ag+ on DHP binding and SH reactivity of the partially purified Ca`channel.…”

Effects of extracellular calcium and calcium channel blocker on silver-induced contractures in frog skeletal muscle fibers.

“…This mechanism is well established as the Ca2+-induced Ca2 + release one, since the original works of ENDO et al (1970) and FORD and PODOLSKY (1970). On the other hand, we found that similar amounts of Ag+ used above induced tonic contracture in single skeletal muscle fibers immersed in a solution containing more than 0.2 mM of Ca2 + (OBA and HOTTA, 1985a). These findings suggest that these Ag+-induced contractures may be atrributed to external Ca2 + or T-tubular membrane bound Ca2 + .…”

“…In either case, the maximum concentration of diltiazem used here (100 jiM) would abolish most Cat + currents which flow across the T-tubular membranes. Furthermore, our previous study showed that 5jM Ag+ caused the contracture in fibres treated for more than 30 min with Ca2+-free solution containing 3 mM EGTA in which T-tubular membrane bound Ca2 + would largely be removed (OBA and HOTTA, 1985a). These findings, therefore, suggest that the Ca2 + -induced Ca2 + release mechanism does not seem to be involved in the initiation of Ag+-induced phasic contracture.…”