The main COX-1 mediated product of platelets which causes platelet aggregation, vascular proliferation and vasoconstriction.
Thromboxanes produced by platelets are vasoconstrictors and facilitate platelet aggregation.
Cyclooxygenase-one and cyclooxygenase-2 are isoenzymes that catalyze the conversion arachidonic acid to prostaglandin H2, the initial step in prostanoid synthesis that leads to the formation of thromboxane A2, PGI2, anf PGE2.
Under physiological conditions platelet thromboxane production is driven primarily by Cox-1, and fewer than 10% of normal platelets have Cox-2.
Cyclooxygenase-2 is expressed in young platelets and the megakaryocytes.
Thromboxane A2 (TXA2) refers to a type of thromboxane that is produced by activated platelets during hemostasis and has prothrombotic properties:
It stimulates activation of new platelets as well as increases platelet aggregation.
Thromboxane A2 is activated by the thromboxane receptor, which results in platelet-shape change, activation of integrins, and platelet degranulation.
Circulating fibrinogen binds these receptors on adjacent platelets, further strengthening the clot.
It is a known vasoconstrictor.
Thromboxane A2 is important during tissue injury and inflammation.
It is also regarded as responsible for Prinzmetal’s angina.
TXA2 is generated from prostaglandin H2 by thromboxane-A synthase.
Aspirin irreversibly inhibits platelet cyclooxygenase 1 preventing the formation of prostaglandin H2, and therefore thromboxane A2.
TXA2 is unstable in aqueous solution, since it is hydrolyzed within about 30 seconds to the biologically inactive thromboxane B2.
TXA2 has a very short half-life and primarily functions as an autocrine or paracrine mediator in the nearby tissues surrounding its site of production.