[Platelet physiology. Advances in platelet reactivity. Review].
Platelets are blood cells that participate in the human primary hemostatic mechanism. Platelets need to be activated to perform all their functions and this activation can be initially produced after an endothelial injury that exposes subendothelial structures to the blood flow. Platelet adhesiveness can also occur by the intervention of high shear forces of the blood stream leading to the attachment of platelets to the subendothelium, forming a monolayer with platelet shape changes and pseudopod emission, that covers all the exposed subendothelial surface. Adhesiveness results from the participation of three components: Glycoprotein Ib, von Willebrand factor and collagen. Fibronectin and vitronectin can also participate in this process. Aggregation (platelet-platelet interaction) has as the final purpose to produce a platelet thrombi that constitutes the primary hemostatic plug. Aggregation involves a sequence of biochemical reactions that are initiated by the contact of an agonist agent (ADP, collagen, thrombin) with receptors on the platelet membrane, this is followed by the fibrinogen binding to Glycoprotein IIb/IIIa complex serving as a link with other surrounding platelets, the aggregation process is then amplified and becomes irreversible with the secretion of the platelet intragranular substances through the release reaction. These series of reactions have their own mechanisms of control that regulate or modulate platelet activation as the Ca2+/cAMP relationship, the balance between PGI2 and TxA2 and the enzymatic system of kinases and phosphatases. The relationship between platelets and other blood cells such as erythrocytes and leukocytes probably modulate the platelet aggregatory response during a vascular injury promoting mechanisms of thrombogenesis and wound healing. On the other hand, the multiple compounds released by the endothelial cell that inhibit platelet function, specially prostacyclin (PGI2) and recently the endothelial derived relaxing factor (EDRF) or nitric oxide have focused new understanding on the physiologic role of platelets in the control of hemostatic and thrombotic processes.
Vizcaíno-Salazar
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Instituto de Investigaciones Clínicas, Facultad de Medicina, Universidad del Zulia, Maracaibo, Venezuela.
D000818:Animals; D016718:Arachidonic Acid / Q000502:physiology; D001792:Blood Platelets / Q000201:enzymology / Q000502:physiology*; D002118:Calcium / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000502:physiology; D000242:Cyclic AMP / Q000502:physiology; D004730:Endothelium, Vascular / Q000166:cytology; D004912:Erythrocytes / Q000166:cytology; D006801:Humans; D007962:Leukocytes / Q000166:cytology; D010716:Phosphatidylinositols / Q000502:physiology; D015539:Platelet Activation; D010973:Platelet Adhesiveness; D010974:Platelet Aggregation; D010980:Platelet Membrane Glycoproteins / Q000737:chemistry / Q000502:physiology; D015398:Signal Transduction
D015815:Cell Adhesion Molecules; D010716:Phosphatidylinositols; D010980:Platelet Membrane Glycoproteins; D016718:Arachidonic Acid; D000242:Cyclic AMP; D002118:Calcium
Fisiología plaquetaria. Avances en la reactividad plaquetaria. Revisión.