Summary. The inward membrane current was recorded under voltage clamp from nonbursting neurons of the snail Helix pomatia in Na-free solutions containing Ba ions but no other divalent cations. The inward current was separated into two components: (i) an early fast inactivating component and (ii) a smaller long-lasting component. Both components were dependent on the external Ba concentration. It is concluded that both components of the inward current are carried by Ba ions. The activation of the early fast inactivating component of the inward current occurred at more positive membrane potential than that of the long-lasting component. The shape of the inactivation curve for the peak value of the inward current was similar to that for the long-lasting component. The potentials of half-inactivation for the peak value of the inward current and for its long-lasting component were -28 and -22mV, respectively. The blocking effect of Co ++ on the early fast inactivating component was substantially greater. In some neurons after treatment with 15 mg Co + § only the long-lasting component was recorded. The activation kinetics of the long-lasting component of the inward current were analyzed using the Hodgkin-Huxley equations. The results could be explained by assuming that two components of the inward current in Na-Ca-free solution with Ba ions flowed through the two different channels. The significance of the long-lasting inward current for the normal spike generation is discussed.

The effects of local anaesthetic tertiary amines (procaine, lignocaine and tetracaine) as well as neutral (benzocaine) and permanently charged (QX‐314) local anaesthetics were studied on the evoked electrical and mechanical activity of the ureter smooth muscle. ‘Low’ concentrations of procaine and lignocaine (0.1‐1 mM) at pH 7.4 increased the duration of the slow plateau component of the evoked action potentials. The amplitude of the phasic contraction was consequently increased within the first 5 min of exposure. Tetracaine 0.1 mM caused a transient increase in the duration of the plateau and amplitude of the phasic contraction within the first 1–2 min only. The stimulant action of the local anaesthetics was greatly reduced in the presence of tetraethylammonium (TEA). All the tertiary local anaesthetics caused depolarization of the membrane accompanied by an increase in the size of the electrotonic potentials. Lignocaine normally initiated the discharge of spontaneous action potentials. High concentrations of lignocaine (5 mM) and tetracaine (0.5 mM) caused complete inhibition of the evoked action potentials and phasic contractions. Procaine 5 mM predominantly inhibited the contractile responses. The permanently charged local anaesthetic QX‐314 (1 mM) caused an increase in the duration and amplitude of the plateau, increasing the number of spikes and the amplitude and duration of the phasic contraction. It also depolarized the ureter smooth muscle cells increasing the size of electronic potentials. The neutral local anaesthetic benzocaine at 1 mM caused a reversible selective blockade of the plateau component of the evoked action potential and a gradual reduction in the amplitude of the phasic contraction. No change in either the membrane potential or the membrane conductance was observed. High pHo (pH 9) significantly increased while low pHo (pH 6) decreased the inhibitory action of procaine and lignocaine but did not alter the effects of benzocaine and QX‐314. Benzocaine caused a relaxation of the high‐K‐induced contraction, preferentially blocking the tonic component, whereas QX‐314 had no effect on the KCl‐contracture of the ureter muscle. Two sites of action in the ureter smooth muscle cell membrane for local anaesthetics are suggested. One site interacts with local anaesthetics in a charged form, while the other one interacts with those in a lipid‐soluble neutral form. The charged form of local anaesthetics has a TEA‐like action, while the neutral form predominantly causes blockade of ‘slow’ Na/Ca channels.

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