Primary coagulation involves the 1) vasculature and 2) platelets:
- The blood vessel wall has an innate ability to constrict when damaged, resulting in decreased blood flow to the damaged area. Endothelin is a vasoconstrictor involved in this process. This is physiologically advantageous, in that it both decreases blood flow to a damaged area and allows blood to be “rerouted” so the body can continue to provide tissues with a blood supply. In addition, the damage to the blood vessel wall results in the exposure of two important cell wall components, von Willebrand factor (vWF) and collagen.
- Platelets, the second component of primary coagulation, are fragments of megakaryocytes from the bone marrow that circulate in the vasculature. When the cell wall becomes damaged, platelets adhere to the exposed vWF and collagen, essentially gluing themselves at the site of vessel injury. The platelets then become activated and secrete thromboxane A2 and ADP, components which result in the activation and aggregation of more platelets. Activated platelets also secrete substances that inhibit the body’s natural anticoagulant mechanisms. Once enough platelets have aggregated at the site of injury, a platelet plug forms. After the platelet plug has formed, secondary coagulation comes into play.