Platelet aggregation induced by equinatoxin.

Equinatoxin, isolated from Actinia equina, caused aggregation of washed rabbit platelets at a concentration as low as 0.01 ng/ml. ATP was released, but no formation of thromboxane B2 in challenged platelets. The aggregation was resistant to indomethacin or creatine phosphate/creatine phosphokinase or PAF antagonist. The aggregation was inhibited by imipramine, sodium nitroprusside, mepacrine, theophylline, prostaglandin E1 and EDTA. However, heparin and tetracaine were without any inhibitory effect. Verapamil suppressed both the aggregation and release reaction caused by equinatoxin in calcium concentrations from 0.01 to 15 mM. High concentrations of equinatoxin caused progressive cell lysis. It is concluded that equinatoxin-induced platelet aggregation is independent of ADP, thromboxane or PAF pathway. Phosphoinositide breakdown by phospholipase C is postulated to accomplish this phospholipase A2-independent platelet aggregation by equinatoxin.