Platelet aggregation is caused by all, except

ADP, Thrombin, Epinephrine, TxA2 promote platelet aggregation whereas ADPase, NO, PGI2, PGE2 inhibit platelet aggregation. All of the aggregating agents, including thrombin, collagen, ADP, and others such as platelet-activating factor, an inside-out signaling pathway, modify the platelet surface glycoprotein complex GPIIb-IIIa (aIIbb3) so that the receptor has a higher affinity for fibrinogen or von Willebrand factor. Molecules of divalent fibrinogen or multivalent von Willebrand factor then link adjacent activated platelets to each other, forming a platelet aggregate. von Willebrand factor-mediated platelet aggregation occurs under conditions of high shear stress. Some agents, including epinephrine, serotonin, and vasopressin, exe synergistic effects with other aggregating agents.