SUMMARY1. The effects of perchlorate (Cl04-) on contraction have been studied in rat soleus muscle fibres using (i) potassium (K+) contracture and (ii) two-microelectrode-point voltage clamp techniques.2. Membrane potentials (l') at all external [K+] were 3-5 mV more negative in CO4-. The hyperpolarization could not be attributed to a change in Na', K+, or C1-permeability, or to an effect on the Na+-K' pump.3. C104-shifts the voltage dependence of tension activation, and contraction threshold, to more negative membrane potentials without altering maximrum tension. Consequently, twitches and submaximal K+ contractures were potentiated, whereas tetanic contractions and 200 mM-K+ contractures were unaltered.4. The decay of K+ contractures during steady depolarization with C104 developed a slow exponential phase with an average time constant of 6 05 + 0 76 min at -38 mV, and 1P68 + 0415 min at -19 mV. This slow component was (a) under the rapid control of the surface t' and (b) did not depend on external Ca2+.5. Inactivation of E-C coupling was measured with a test 200 mm-K+ depolarization following 3-10 min depolarizations in conditioning solutions containing 20-120 mM-K+. C104-induced a negative shift in the curve-relating test K+ contracture amplitude to conditioning Vm but did not alter the rate of repriming of tension upon repolarization.6. The results suggest that C104-increases the amount of activator produced during depolarization and thus allows the slow inactivation step in excitationcontraction (E-C) coupling to be reflected in the decay of K+ contracture tension.7. A 'perchlorate contracture', which did not depend on the activation of E-C coupling, was observed. The contracture depended on external Ca2+, but not on voltage-dependent Ca2+ channels or Na+-Ca2+ exchange.