second type of membrane channel. The DTS contains an electron-dense material originating from the rough endoplasmic reticulum of the megakaryocyte, which serves as a storage site for calcium ions. DTS channels do not connect with the surface of the platelet; however, both the OCS and DTS fuse in various areas of the platelet to form membrane complexes that are important in regulation of the intraplatelet calcium concentration.
Platelets function in continuous surveillance of blood vessels, blood clot formation, and repair of injured tissue.
Platelets are involved in several aspects of hemostasis (control of bleeding). They continuously survey the endothelial lining of blood vessels for gaps and breaks. When a blood vessel wall is injured or broken, the exposed connective tissue at the damaged site promotes platelet adhesion. Adhesion of the platelets at the damaged site triggers their degranulation and release of serotonin, ADP, and thromboxane A2.
Serotonin is a potent vasoconstrictor that causes the vascular smooth muscle cells to contract, thereby reducing local blood flow at the site of injury. Adenosine diphosphate (ADP), a nucleotide, and the signaling molecule thromboxane A2, are responsible for further aggregation of platelets into a primary hemostatic plug. The mass of aggregated platelets stop extravasation of blood.
At the same time, the activated platelets release their  and  granules, which contain among other substances coagulation factors such as platelet thromboplastic factor (PF3) and additional serotonin.
The glycocalyx of the platelets provides a reaction surface for the conversion of soluble fibrinogen into fibrin. Fibrin then forms a loose mesh over the initial plug and is further
FIGURE 10.15 • Scanning electron micrograph of blood clot.
High-magnification scanning electron micrograph shows initial stage of blood clot formation. Red blood cells are entrapped in a loose mesh of fibrin fibers that are extensively cross-linked to form impermmable hemostatic plug that prevents movement of cells and fluids from the lumen of the injured vessel. 1,600. (Copyright Dennis Kunkel Microscopy, Inc.) stabilized by covalent cross-links that produce a dense aggregation of fibers (Fig 10.15). Platelets and red blood cells become trapped in this mesh. The initial platelet plug is transformed into a definitive clot known as a secondary hemostatic plug by additional tissue factors secreted by the damaged blood vessel.
After the definitive clot is formed, platelets cause clot retraction, probably as a function of the actin and myosin found in the structural zone of the platelet. Contraction of the clot permits the return of normal blood flow through the vessel.  Finally, after the clot has served its function, it is lysed by plasmin, a fibrinolytic enzyme that circulates in the plasma in an inactive form known as plasminogen. The hydrolytic enzymes released from the granules assist in this process. The activator for plasminogen conversion, tissue plasminogen activator (TPA), is derived principally from endothelial cells. A synthetic form of TPA is currently used as an emergency treatment to minimize the damage caused by clots that lead to strokes.
An additional role of platelets is to help repair the injured tissues beyond the vessel itself. Platelet-derived growth factor released from the  granules stimulates smooth muscle cells and fibroblasts to divide and allow tissue repair.