Endogenous mediators and thrombophilia.
Platelet function is a balance between factors determined at thrombopoiesis and prothrombotic and antithrombotic mediators from the vascular wall. Nitric oxide is a crucial vasodilator and inhibitor of platelet activation synthesized constitutively by the vascular endothelium. In some pathological states this synthesis may be impaired leading to a prothrombotic state. In other situations, synthesis may be increased by a second inducible enzyme. Nitric oxide synergizes with other antithrombotic vasodilators such as prostacyclin and is opposed by prothrombotic vasoconstrictor mediators such as thromboxane. Platelets are anucleate and their reactivity is partly determined at thrombopoiesis by their progenitor cell, the megakaryocyte. In thrombotic states, such as myocardial infarction, larger, more reactive platelets from larger megakaryocytes are observed.
Smith
R E
RE
Department of Medicine, King's College School of Medicine and Dentistry, London, UK.
Martin
J F
JF
D000818:Animals; D001792:Blood Platelets / Q000502:physiology*; D048429:Cell Size; D016232:Endothelins / Q000502:physiology; D004730:Endothelium, Vascular / Q000503:physiopathology; D011464:Epoprostenol / Q000502:physiology*; D006706:Homeostasis; D006801:Humans; D008533:Megakaryocytes / Q000648:ultrastructure; D009569:Nitric Oxide / Q000502:physiology*; D015539:Platelet Activation / Q000502:physiology; D013927:Thrombosis / Q000503:physiopathology*; D013931:Thromboxanes / Q000502:physiology
D016232:Endothelins; D013931:Thromboxanes; D009569:Nitric Oxide; D011464:Epoprostenol