description
Under normal conditions the vascular endothelium supports vasodilation, inhibits platelet adhesion and activation, suppresses coagulation, enhances fibrin cleavage and is anti-inflammatory in character. Under acute vascular trauma, vasoconstrictor mechanisms predominate and the endothelium becomes prothrombotic, procoagulatory and proinflammatory in nature. This is achieved by a reduction of endothelial dilating agents: adenosine, NO and prostacyclin; and by the direct action of ADP, serotonin and thromboxane on vascular smooth muscle cells to elicit their contraction (Becker et al. 2000). Cyclooxygenase-2 (COX-2) and endothelial nitric oxide synthase (eNOS) are primarily expressed in endothelial cells. Both are important regulators of vascular function. Under normal conditions, laminar flow induces vascular endothelial COX-2 expression and synthesis of Prostacyclin (PGI2) which in turn stimulates endothelial Nitric Oxide Synthase (eNOS) activity. PGI2 and NO both oppose platelet activation and aggregation, as does the CD39 ecto-ADPase, which decreases platelet activation and recruitment by metabolizing platelet-released ADP

external resources
NCBI:1269341
REACTOME:R-HSA-418346
PUBMED:10798271

genes
APOB , ATP2A1 , ATP2A2 , ATP2A3 , ATP2B1 , ATP2B2 , ATP2B3 , ATP2B4 , CALM1 , CALM2 , CALM3 , MAPK14 , FGR , GNAS , GNB1 , GNB2 , GNB3 , GNG3 , GNG4 , GNG5 , GNG7 , GNG10 , GNG11 , GNGT1 , GNGT2 , GUCY1A2 , GUCY1A1 , GUCY1B1 , ITPR1 , ITPR2 , ITPR3 , KCNMA1 , KCNMB1 , NOS1 , NOS2 , NOS3 , P2RX1 , P2RX3 , P2RX4 , P2RX5 , P2RX7 , PAFAH2 , PDE1A , PDE2A , PDE3A , PDE3B , PDE9A , PDE1B , PECAM1 , PLA2G4A , PPP2CA , PPP2CB , PPP2R1A , PPP2R1B , PPP2R5A , PPP2R5B , PPP2R5C , PPP2R5D , PPP2R5E , PRKG1 , PRKG2 , PTGIR , PTPN6 , PTPN11 , SLC8A2 , SLC8A1 , SLC8A3 , SRI , STIM1 , TRPC3 , TRPC6 , LRP8 , PDE5A , P2RX6 , KCNMB2 , MRVI1 , GNB5 , PDE10A , P2RX2 , KCNMB3 , KCNMB4 , PDE11A , GNG13 , GNG2 , GNG12 , TRPC7 , GNB4 , ORAI2 , ORAI1 , GNG8 , MIR4687 ,