Description:
<jats:p><jats:list list-type="explicit-label">
<jats:list-item><jats:p>The effects of bisaramil on sodium currents in rat isolated cardiac myocytes were examined by use of tight‐seal, whole‐cell patch clamp techniques. Bisaramil produced a concentration‐dependent, readily reversible reduction in peak transient sodium current. When the sodium current was evoked at 3 s intervals the estimated ED<jats:sub>50</jats:sub> for bisaramil was about 11 μ<jats:sc>m</jats:sc>.</jats:p></jats:list-item>
<jats:list-item><jats:p>Bisaramil (16 μ<jats:sc>m</jats:sc>) produced a shift in the inactivation curve to hyperpolarized potentials of about 10 mV, but produced no change in the voltage‐dependence of activation.</jats:p></jats:list-item>
<jats:list-item><jats:p>The block of the sodium current by bisaramil showed a profound use‐dependence. A concentration of 10 μ<jats:sc>m</jats:sc> produced a considerable block of the current with repeated stimulation. The recovery from block was biphasic, showing fast and slow components which had time constants of about 40 ms and 5 s respectively.</jats:p></jats:list-item>
<jats:list-item><jats:p>Bisaramil produced little tonic block of the sodium current at concentrations of 100 μ<jats:sc>m</jats:sc>; at 300 μ<jats:sc>m</jats:sc> it produced tonic block of around 50%, with extreme use‐dependence.</jats:p></jats:list-item>
<jats:list-item><jats:p>Bisaramil appeared not to interact primarily with the inactivated form of the channel, since lengthening the depolarizing pulses did not affect the degree of block produced.</jats:p></jats:list-item>
</jats:list></jats:p>