Thromboxane A2

Source: Wikipedia, the free encyclopedia.
Thromboxane A2
Identifiers
3D model (
JSmol
)
ChEBI
ChemSpider
IUPHAR/BPS
KEGG
MeSH Thromboxane+A2
UNII
  • InChI=1S/C20H32O5/c1-2-3-6-9-15(21)12-13-17-16(18-14-20(24-17)25-18)10-7-4-5-8-11-19(22)23/h4,7,12-13,15-18,20-21H,2-3,5-6,8-11,14H2,1H3,(H,22,23)/b7-4-,13-12+/t15-,16+,17+,18-,20+/m0/s1 ☒N
    Key: DSNBHJFQCNUKMA-SCKDECHMSA-N ☒N
  • CCCCC[C@@H](/C=C/[C@@H]1[C@H]([C@@H]2C[C@@H](O2)O1)C/C=C\CCCC(=O)O)O
Properties
C20H32O5
Molar mass 352.471 g·mol−1
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)

Thromboxane A2 (TXA2) is a type of

Prinzmetal's angina
.

Receptors that mediate TXA2 actions are thromboxane A2 receptors. The human TXA2 receptor (TP) is a typical G protein-coupled receptor (GPCR) with seven transmembrane segments. In humans, two TP receptor splice variants – TPα and TPβ – have so far been cloned.

Synthesis and breakdown

TXA2 is generated from

cyclooxygenase 1 preventing the formation of prostaglandin H2, and therefore thromboxane A2. Contrastly, TxA2 vascular tissue synthesis is stimulated by angiotensin II which promotes cyclooxygenase I's metabolism of arachidonic acid. An angiotensin II dependent pathway also induces hypertension and interacts with TxA2 receptors.[6]

TXA2 is very unstable in aqueous solution, since it is hydrated within about 30 seconds to the biologically inactive

11-dehydrothromboxane B2 levels are used to indirectly measure TXA2 production.[9][10]

Eicosanoid synthesis.

References