Platelets circulate within the blood until they encounter a damaged endothelial surface. Contact with exposed subendothelial collagen fibres, in the presence of factor VIII and von Willebrands factor, stimulates adhesion and activation. ADP released locally at the site of damage may have the same effect. The intracellular messenger, protein kinase C, is increased in concentration and arachidonic acid is newly metabolised to active moieties.
Rapid cytoskeletal rearrangement changes the platelet shape from disciform to stellate with pseudopods emerging from its surface.
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