Thromboxane

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Thromboxane A2

Thromboxane B2

Thromboxane is a member of the family of lipids known as eicosanoids. The two major thromboxanes are thromboxane A2 and thromboxane B2.

Thromboxane is named for its role in clot formation (thrombosis).

Production

Enzymes and substrates associated with thromoboxane and prostacyclin synthesis.

Eicosanoid synthesis.

It is produced in platelets by thromboxane-A synthase from the endoperoxides produced by the cyclooxygenase (COX) enzyme from arachidonic acid.

Mechanism

Thromboxane acts by binding to any of the thromboxane receptors, G-protein coupled receptors coupled to the G protein G_q^[1].

Functions

Thromboxane is a vasoconstrictor and a potent hypertensive agent, and it facilitates platelet aggregation.

It is in homeostatic balance in the circulatory system with prostacyclin, a related compound. The mechanism of secretion of thromboxanes from platelets is still unclear.

Role of A2 in platelet aggregation

Thromboxane A₂ (TXA₂), produced by activated platelets, has prothrombotic properties, stimulating activation of new platelets as well as increasing platelet aggregation.

Platelet aggregation is achieved by mediating expression of the glycoprotein complex GP IIb/IIIa in the cell membrane of platelets. Circulating fibrinogen binds these receptors on adjacent platelets, further strengthening the clot.

Pathology

It is believed that the vasoconstriction caused by thromboxanes plays a role in Prinzmetal's angina.

Suppression

The widely used drug aspirin acts by inhibiting the ability of the COX enzyme to synthesize the precursors of thromboxane within platelets.

It inhibits the COX enzyme both non-competitively and irreversibly.

The side effect of this is that people who regularly take aspirin will suffer from excessive bleeding whenever the skin is perforated.

External links

• MeSH Thromboxanes

de:Thromboxanfr:Thromboxane ja:トロンボキサン

Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .