Platelet structural physiology has contributed significantly to our understanding of basic mechanisms of platelet function in hemostasis and thrombosis. Current evidence indicates that platelets are a form of muscle cell with specialized capabilities for secretion and adhesion-aggregation. Activation of the discoid cell by any agent appears to involve a perturbation of the membrane resulting in movement of calcium from the cell wall to the interior. The calcium flux stimulates phospholipase A2 to cleave arachidonic acid from platelet phospholipids starting the cascade of prostaglandin synthesis. In addition, the movement of calcium to the cytoplasm initiates contraction leading to shape change. Products formed during prostaglandin synthesis, particularly thromboxane A2, act as ionophores to transport additional calcium from the dense tubular system to the cytoplasm amplifying the wave of contraction. Alterations in organelle membranes result in their fusion with channels of the open canalicular system. The contractile wave causes extrusion of secretory products which stimulate other platelets to become involved in formation of irreversible aggregates in vitro and hemostatic plugs in vivo. Mechanisms regulating platelet stimulation-contraction-secretion coupling are currently under investigation.