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Pharmacological properties of the interaction of a sea anemone polypeptide toxin with cardiac cells in culture.

Three approaches have been used to analyze the mechanism of action of a sea anemone neurotoxin on cultured chick embryonic cardiac cells: 1) electrophysiological measurements; 2) simultaneous recordings of contraction properties; and 3) measurements of cationic influx of 22Na+ and 45Ca++ The chick embryo cell cultures consisted of 3-day aggregates and monolayer cultures which have electrophysiological properties of the early embryonic type and 16-day aggregates which have electrophysiological properties of the adult type. All types of cardiac cell cultures responded similarly to exposure to the 47 amino acid long sea anemone toxin extracted from Anemonia sulcata. The polypeptide toxin provoked action potentials with a plateau phase of long duration, a slowing down of the beating rate and simultaneously with the prolonged action potential an increase in amplitude and duration of cardiac contractions. Our results indicate: 1) that the site of action of the sea anemone toxin on cardiac cell is the Na+ channel as in other excitable system; 2) that the sea anemone toxin can reveal unexpressed ("silent") fast Na+ channels in cardiac cells of the early embryonic type; and 3) that the increase in amplitude and duration of cardiac contractions caused by the polypeptide toxin is most probably due to an indirect activation of the Na+-Ca++ exchange system.