As discussed earlier, a break in the vessel endothelium leads to exposure of collagen and the vessel's subendothelial layer. Ruptured endothelial cells leak ADP and serotonin, the chemical triggers that induce platelet adhesion, which is the next step in the sequence of hemostatic events. Circulating platelets are drawn to the area by those liberated chemical signals and begin to physically attach themselves to the rough, damaged surfaces of the damaged vessel wall.
Once platelets begin adhering to the damaged area of the vessel wall, the platelets start to change their shape and functionality through a process called platelet activation. The activated platelets undergo various changes, including the alteration of their surface receptors as they prepare to create a primary platelet plug. At this time, the platelets also release the contents of their granules through a process called platelet secretion which helps to attract more platelets to the site of injury as a positive feedback mechanism.
As platelets continue to arrive and bind to the exposed collagen and basement membrane, a rudimentary barrier begins to form, as the platelets themselves serve to fill in the breached vessel wall. The process by which platelets bind to one another is referred to as platelet aggregation. Platelet aggregation is vital because it allows for a primary platelet plug to be formed. The platelet plug is the structure responsible for plugging the hole in the vessel wall, preventing further blood loss. The formation of the platelet plug signals the end of primary hemostasis, and serves to initiate upcoming processes associated with secondary hemostasis.
