title: A mechanistic interpretation of the action of toxin II from Anemonia sulcata on the cardiac sodium channel.
abstract: 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.
mesh_terms: 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*
chemical_list: D003064:Cnidarian Venoms; D007473:Ion Channels; C028800:toxin II (Anemonia sulcata); D012964:Sodium