DP1 function to counteract each other. PGE2: EP-(PGE2) (PGE2 receptor) EP1-(PGE2) (PTGER1) – ; EP1 is a receptor for prostaglandin E2; relative potencies in binding to and stimulating EP1 are PGE2>PGF2α=PGI2>PGD2=TXA2 (http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=346&familyId=58&familyType=GPCR). EP1 activation is associated with the promotion of inflammation, particularly in the area of inflammation-based pain perception, and asthma, particularly in the area of airways constriction. EP2-(PGE2) (PTGER2) – ; EP2 is a receptor for prostaglandin E2; relative potencies in binding to and stimulating EP2 are PGE2>PGF2α=PGI2>PGD2=TXA2 (http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=341). EP2 activation is associated with the suppression of inflammation and inflammation-induced pulmonary fibrosis reactions as well as allergic reactions. EP3-(PGE2) (PTGER3) – ; EP3 is a receptor for prostaglandin E2; relative potencies in binding to and stimulating EP3 are PGE2>PGF2α=PGI2>PGD2+TXA2 (http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=342). Activation of EP3 is associated with the suppression of the early and late phases of allergic responses; EP3 activation is also responsible for febrile responses to inflammation. EP4-(PGE2) (PTGER4) – ; EP4 is a receptor for prostaglandin E2; relative potencies in binding to and stimulating EP4 are PGE2>PGF2α=PGI2>PGD2=TXA2 (http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=343). EP4, particularly in association with EP2, activation is critical for the development of arthritis in different animal models. PGF2α: FP-(PGF2α) (PTGFR) – ; FP is the receptor for prostaglandin F2 alpha; relative potencies in binding to and stimulating FP are PGF2α>PGD2>PGE2>PGI2=thromboxane A2 (http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=344). This receptor is the least selective of the prostanoid receptors in that both PGD2 and PGE2 bind to and stimulate it with potencies close to that of PGF2α. FP has two splice variants, FPa and FPb, which differ in the length of their C-terminus tails. PGF2α-induced activation of FP has pro-inflammatory effects as well as roles in ovulation, luteolysis, contraction of uterine smooth muscle, and initiation of parturition. Analogs of PGF2α have been developed for estrus synchronization, abortion in domestic animals, influencing human reproductive function, and reducing intraocular pressure in glaucoma. PGI2 (prostacyclin): IP-(PGI2) (PTGIR) – ; IP is the receptor for prostacyclin I2; relative potencies in binding to and stimulating IP are: PGI2>>PGD2= PGE2=PGF2α>TXA2 (http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=345). Activation of IP is associated with the promotion of capillary permeability in inflammation and allergic responses as well as partial suppression of experimental arthritis in animal models. IP is expressed in at least three alternatively spliced isoforms which differ in the length of their C-terminus and which also activate different cellular signaling pathways and responses. TXA2 (thromboxane): TP-(TXA2) (TBXA2R) – ; TP is the receptor for thromboxane A2; relative potencies in