Prostanoid receptors are activated by the endogenous ligands prostaglandin (PG) D2, PGE2, PGF2α, PGH2, prostacyclin (PGI2) and thromboxane A2. Cyclooxygenase (COX) converts arachidonic acid to PGH2, from which the other prostaglandins are synthesized. Prostanoid receptors are a family of nine G-protein-coupled receptors that have distinct tissue distributions and actions.
- DP receptors (DP1-2) are coupled to Gαs. They are expressed in the small intestine, lung, stomach and uterus. Activation of DP1 results in inhibition of platelet activation and vasodilation; they are also involved in sleep regulation. DP2 activation leads to immune cell activation.
- EP receptors (EP1-4) are a diverse group of prostanoid receptors. EP1 receptors are restricted to the kidney, lung and stomach, and induce smooth muscle contraction. EP2 and EP4 couple to Gαs and induce smooth muscle relaxation. EP3 is an inhibitory receptor that prevents smooth muscle relaxation.
- FP receptors are coupled to Gαq. They are abundant in the corpus luteum, where they are involved in luteolysis.
- IP receptors are coupled to Gαs and are involved in pain mediation, relaxation of vascular smooth muscle, inhibition of platelet aggregation and they contribute to cardiovascular health.
- TP receptors can be coupled to both Gαq and Gαi. They are expressed abundantly in highly vascular tissues such as the kidney and heart, and immune-related organs such as the thymus and spleen. They mediate smooth muscle contraction and platelet aggregation.
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Literature for Prostanoid Receptors
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