A minor effect on sodium channels at higher concentrations has also been seen, but these effects appear to vary between species.
Other hainantoxins bind at site 3 of the sodium channels.
They act by binding to fast sodium channels from within (in an open state).
The class I antiarrhythmic agents interfere with the sodium channel.
The sodium channels close at the peak of the action potential, while potassium continues to leave the cell.
These toxins are thought to operate by opening sodium channels.
After a short while, the open sodium channels inactivate and become refractory.
Inhibitors of sodium channels have also been found in this venom.
The actions of these two drugs are mediated principally through sodium channels.
The fast sodium channels are voltage-dependent and have a very important role in cardiac action potential as explained above.
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