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Prostacyclin is produced in endothelial cells, which line the walls of arteries and veins, [14] from prostaglandin H 2 (PGH 2) by the action of the enzyme prostacyclin synthase. Although prostacyclin is considered an independent mediator, it is called PGI 2 (prostaglandin I 2 ) in eicosanoid nomenclature, and is a member of the prostanoids ...
The prostacyclin receptor, also termed the prostaglandin I 2 receptor or just IP, is a receptor belonging to the prostaglandin (PG) group of receptors. IP binds to and mediates the biological actions of prostacyclin (also termed prostaglandin I 2 , PGI 2 , or when used as a drug, epoprostenol).
Similarly, prostacyclin (PGI 2) synthase (PGIS) converts PGH 2 into PGI 2. A thromboxane synthase has also been identified. Prostaglandin-F synthase (PGFS) catalyzes the formation of 9α,11β-PGF 2α,β from PGD 2 and PGF 2α from PGH 2 in the presence of NADPH.
Prostaglandin receptors or prostanoid receptors represent a sub-class of cell surface membrane receptors that are regarded as the primary receptors for one or more of the classical, naturally occurring prostanoids viz., prostaglandin D2, (i.e. PGD2), PGE2, PGF2alpha, prostacyclin (PGI2), thromboxane A2 (TXA2), and PGH2. [1]
All other prostanoids originate from PGH (as PGH 1, PGH 2, or PGH 3). The image at right shows how PGH 2 (derived from Arachidonic acid) is converted: By PGE synthetase into PGE2 (which in turn is converted into PGF2) By PGD synthetase into PGD2; By Prostacyclin synthase into prostacyclin (PGI2) By Thromboxane synthase into thromboxanes TXA
Prostacyclin (PGI 2) is released by endothelium and activates platelet G s protein-linked receptors. This, in turn, activates adenylyl cyclase , which synthesizes cAMP. cAMP inhibits platelet activation by decreasing cytosolic levels of calcium and, by doing so, inhibits the release of granules that would lead to activation of additional ...