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
,
