<prompt> Platelet aggregation is caused by all, exceptThromboxane A2EpinephrineProstacyclin PGI2Thrombin  <response>: 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. 