Ca²⁺‐dependent aggregation of rabbit platelets induced by maitotoxin, a potent marine toxin, isolated from a dinoflagellate

Administration of maitotoxin (MTX), a dinoflagellate toxin, caused aggregation of rabbit washed platelets. The cytosolic Ca²⁺ concentration ([Ca²⁺]_i), measured by fura‐2 fluorescence technique, was also increased by the presence of MTX. Rates of aggregation response and [Ca²⁺]_i‐increase were dependent on tested concentrations (3–100 ng ml⁻¹) of the toxin. The MTX‐induced platelet aggregation and [Ca²⁺]_i‐increase were totally abolished in a Ca²⁺‐free solution. The successive administration of Ca²⁺ in the presence of MTX elicited the aggregation and increase in [Ca²⁺]_i. Ba²⁺ was capable of substituting for Ca²⁺ in the MTX‐induced platelet aggregation. In the presence of external Ca²⁺, transition metals, Co²⁺, Cd²⁺ and Ni²⁺, inhibited the aggregation response to MTX. Organic calcium antagonists (verapamil and nifedipine) as well as a cyclo‐oxygenase‐inhibitor (aspirin) did not apparently inhibit the aggregation response to MTX, except for a high concentration (10⁻⁵ m) of verapamil, while procaine (10 mm) reduced the rate of platelet aggregation. MTX also elicited a release of ATP from platelets, which was abolished in the absence of external Ca²⁺. In contrast, thrombin 0.5 unit ml⁻¹ could elicit platelet shape change, [Ca²⁺]_i‐increase and ATP‐release in the absence of external Ca²⁺. These results suggest that the MTX‐induced platelet activation is caused by an enhanced Ca²⁺‐influx presumably through voltage‐independent Ca²⁺ channels on the plasma membrane. 1993 British Pharmacological Society