A mechanistic interpretation of the action of toxin II from Anemonia sulcata on the cardiac sodium channel.
Cardiac sodium channels, modified by Anemonia sulcata toxin II, have been analyzed by the patch-clamp method. The open state of the modified sodium channels proved to be prolonged highly significantly and reopening from a closed state denoted c*-state frequently occurred, interrupted by silent periods, denoted i*-state. Activation from the c*-state was apparently not affected by toxin action, whereas activation from the i*-state was markedly prolonged. Upon higher depolarizations toxin-induced sodium channels disappeared and this behaviour has been attributed to dissociation of the toxin from the channel by use of a special pulse-protocol. The onset of the toxin effect on the action potential proved to depend on stimulation, and it is concluded that the toxin binds preferentially to the open (o)-state. Taking together the results, a kinetic scheme is suggested for action of the toxin on the cardiac sodium channel.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D003064:Cnidarian Venoms / Q000494:pharmacology*; D005260:Female; D006321:Heart / Q000187:drug effects; D007473:Ion Channels / Q000187:drug effects*; D007700:Kinetics; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D012964:Sodium / Q000378:metabolism*
D003064:Cnidarian Venoms; D007473:Ion Channels; C028800:toxin II (Anemonia sulcata); D012964:Sodium