Prostacyclin (PGI2) is continuously produced by healthy vascular endothelial cells. It inhibits platelet activation through interaction with the Gs-coupled receptor PTGIR, leading to increased cAMP, a consequent increase in cAMP-dependent protein kinase activity which prevents increases of cytoplasmic [Ca2+] necessary for activation (Woulfe et al. 2001). PGI2 is also an effective vasodilator. These effects oppose the effects of thromboxane (TXA2), another eicosanoid, creating a balance of blood circulation and platelet activation.