The effects of tetracaine and nifedipine on asymmetric charge movement in rabbit muscle fibres were examined to investigate whether mammalian charge movement could be subdivided into several components. Tetracaine (0.05-0.2 mM) stopped contraction in every sternomastoid fibre examined (n = 9) and reduced the asymmetric charge (moved by depolarizing steps to 0 mV) by 15% (S.E. of mean 3%). Tetracaine had little effect on the charge moved at potentials more negative than the threshold potential (established in the absence of the drug). Application of the Ca2+ channel blocker nifedipine (2 or 10 microM), reduced the mean maximum asymmetric charge to 50% (+/- 4) of the control value in twenty-three sternomastoid fibres and to 32% (+/- 5) in four soleus fibres. Increasing the concentration of nifedipine to 120 microM had little further effect. The charge moved at potentials more negative than -60 mV was unaffected by nifedipine. A similar result was found with 30 microM-D600 (two fibres). 10 microM-nifedipine completely blocked Ca2+ currents (external [Ca2+] = 8 mM), but 0.15 microM-nifedipine only had a small effect on either the Ca2+ current or charge movement in the four fibres examined. Contractions could no longer be elicited in eleven of eighteen fibres within 6 min of the application of 2 or 10 microM-nifedipine. However, in the remaining seven fibres contractions could be elicited with unchanged thresholds over 30 min, even in the presence of 50 microM-nifedipine. Nifedipine did not noticeably effect q gamma. It is suggested that nifedipine might prevent contraction only when, for other reasons, the normal release of Ca2+ from the sarcoplasmic reticulum has been disrupted and contraction is dependent on the inflow of external Ca2+. The amount of asymmetric charge moved by depolarizing steps was about 50% greater with a holding potential of -110 mV than with one of -90 mV. This 'extra' charge was not suppressed by nifedipine.