– attachment of cells on a surface at the site of endothelial injury
subendothelial elements (e.g., collagen) are exposed and platelets spread along the surface
interaction of subendothelium, von Willebrand factor (vWF) and GPIb (platelet surface membrane vWF receptor)
– release of granular contents and prostaglandin metabolites (e.g., thromboxane A2) from adherent platelets
these interact with receptors on adjacent platelets and lead to their incorporation into the evolving aggregate
activation by ADP, collagen, epinephrine, etc. causes membrane phospholipase A2 to release arachidonic acid
converted into PGE2/H2
Þ thromboxane A2, a stimulus for amplification of platelet activation
Note: endothelial cells use PGE2/H2 to make PGI2, which counteracts thromboxane A2. However, since these cells have a nucleus, they can produce more phospholipid, whereas platelets cannot. As a result, universal inhibition of prostaglandin synthesis (by aspirin) preferentially disrupts platelet function.
independently, phospholipase C cleaves (PIP2) to inositol triphosphate (IP3) and diacylglycerol (DAG)
IP3 leads to efflux of calcium from the dense tubular system and influx of calcium from the ext. membr.
DAG causes shape change and secretion of granules via activation of protein kinase C
release many substances from the intracellular granules
dense granules: ADP and serotonin (platelet-derived vasoconstrictor)