Platelet aggregation induced by equinatoxin
Related Experiment Video
Updated: Jan 3, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
1Pharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan, R.O.C.
Abstract:
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.
Related Concept Videos
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Clot Retraction and Fibrinolysis
Intracellular Signaling Affects Focal Adhesions
Some...
Anticoagulant Drugs: Low-Molecular-Weight Heparins

