Shape change is the primary event in activated platelets after thrombin stimulation or integrin alphaIIbbeta3-mediated adhesion to fibrinogen. It is followed by granule secretion, aggregation and microvesiculation. Microvesiculation is always preceded by loss of membrane assymetry and procoagulant surface exposure. Major actin cytoskeleton movements are required, regulated by the increase of intracellular calcium concentration, phosphoinositides, GTPases of the Rho family (Cdc42, Rac1 and RhoA) and multimolecular signalling complexes. Platelet shape change consists in Rac1-regulated lamellipodia formation for platelet spreading and in Cdc42-regulated protrusion of filopodia for platelet aggregation to the fibrin network. RhoA stabilizes platelet clots by establishing stress fibers and clustering alphaIIbbeta3 integrins. Microparticles are detected in the vicinity of platelet aggregates. After phosphatidylserine exposure on the outer-leaflet of plasma membrane, mediated by the activation of Ca++-dependent phospholipid scramblase and the inhibition of aminophospholipid translocase, microparticles are shed by budding of the plasma membrane. Budding may depend on the membrane skeleton reorganization and on the restricted activation of proteases such as calpain. Regulators of microvesiculation are still unknown and could represent a target for new pharmacological agents because microvesiculation favors blood coagulation dissemination, arterial thrombosis initiation and expansion after plaque rupture.