Degranulation in platelets results in the release of serotonin and adenosine diphosphate (ADP) from dense granules. Serotonin causes vasoconstriction, while ADP activates additional platelets by binding to GPCR on their surface. Platelet-derived growth factor, VWF, FV, FXIII, and FI are among the other proteins released from α granules. Platelet-activating factor (PAF), an ether phospholipid synthesized by various cell types including endothelial cells and platelets, activates platelets by binding to PAF receptors on their surface. 

When platelets are activated, they undergo a morphologic change from a discoidal shape to a spherical shape with pseudopod-like processes. This change is facilitated by the release of Ca2+ from dense granules. The binding of Ca2+ to calmodulin mediates the activation of myosin light chain kinase, which phosphorylates the myosin light chain. This phosphorylation leads to a major reorganization of the platelet cytoskeleton.

Activation of platelets also causes them to aggregate. Structural changes in a surface receptor called GPIIb/IIIa expose binding sites for fibrinogen. Fibrinogen molecules then link activated platelets together, with a single fibrinogen molecule able to bind to two platelets. Fibrinogen is converted to fibrin by thrombin (FIIa), and this fibrin is covalently cross-linked by factor XIIIa. Fibrin formation strengthens the platelet plug, contributing to secondary hemostasis.

To prevent unnecessary activation of platelets, the intact vascular wall is separated from the blood by a monolayer of endothelial cells. These cells prevent platelet contact with collagen. Additionally, endothelial cells produce prostaglandin I2 (PGI2) and nitric oxide, both of which cause vasodilation. Furthermore, endothelial cells possess a cell surface ADPase that converts ADP to adenosine monophosphate.

In summary, blood clotting (coagulation) is a process that quickly stops bleeding from a damaged blood vessel to maintain a constant blood volume. It involves the formation of a clot (thrombus) consisting of a platelet plug and a fibrin meshwork.
Degranulation also results in release of serotonin and adenosine diphosphate (ADP) from dense granules. Serotonin causes vasoconstriction. ADP binds to GPCR on the surface of platelets, activating additional platelets. [Note: Some antiplatelet drugs, such as clopidogrel, are ADP-receptor antagonists.] Platelet-derived growth factor (involved in wound healing), VWF, FV, FXIII, and FI are among other proteins released from α granules. [Note: Platelet-activating factor (PAF), an ether phospholipid (see p. 202) synthesized by a variety of cell types including endothelial cells and platelets, binds PAF receptors (GPCR) on the surface of platelets and activates them.] 2. Morphologic change: The change in shape of activated platelets from discoidal to spherical with pseudopod-like processes that facilitate platelet–platelet and platelet–surface interactions (Fig. 35.23) is initiated by the release of Ca2+ from dense granules. Ca2+ bound to calmodulin (see p. 133) mediates the activation of myosin light chain kinase that phosphorylates the myosin light chain, resulting in a major reorganization of the platelet cytoskeleton.
C. Aggregation
Activation causes dramatic changes in platelets that lead to their aggregation. Structural changes in a surface receptor (GPIIb/IIIa) expose binding sites for fibrinogen. Bound FI molecules link activated platelets to one another (Fig. 35.24), with a single FI able to bind two platelets. FI is converted to FIa by FIIa and then covalently cross-linked by FXIIIa coming from both the blood and the platelets. [Note: The exposure of PS on the surface of activated platelets allows formation of the Xase complex (VIIIa, IXa, X, and Ca2+) with subsequent formation of FXa and generation of FIIa.] Fibrin formation (secondary hemostasis) strengthens the platelet plug. [Note: Rare defects in the platelet receptor for FI result in Glanzmann thrombasthenia (decreased platelet function), whereas autoantibodies to this receptor are a cause of immune thrombocytopenia (decreased platelet number).]
Unnecessary activation of platelets is prevented because 1) an intact vascular wall is separated from the blood by a monolayer of endothelial cells, preventing the contact of platelets with collagen; 2) endothelial cells synthesize prostaglandin I2 (PGI2, or prostacyclin) and nitric oxide, each of which causes vasodilation; and 3) endothelial cells have a cell surface ADPase that converts ADP to adenosine monophosphate.
V. CHAPTER SUMMARY
Blood clotting (coagulation) is designed to rapidly stop bleeding from a damaged blood vessel in order to maintain a constant blood volume (hemostasis). Coagulation is accomplished through formation of a clot (thrombus) consisting of a plug of platelets and a meshwork of the protein fibrin (Fig. 35.25).