Prostanoids comprising the prostaglandins(PGs) and thromboxanes(TXs) are potent eicosanoid lipid mediators generated by the cyclooxygenase(COX) isozymes. Pros tanoids are quickly released from cells after synthesis and act as local hormones in the vicinity of their production site to maintain local homeostasis. The ability of each pros tanoid to affect various biological responses is dependent on its binding to specific receptors on the plasma membrane. These prostanoid receptors are classified into five basic types, termed DP, EP, FP, IP, and TP receptors, on the basis of their sensitivities to the five primary prostanoids, PGD2, PGE2, PGF2,, PGI2, and TXA2, respectively. Furthermore, there are several receptor subtypes for PGD2 and PGE2. PGD2 acts through two receptors, the DP receptor and the recently identified CRTH2 receptor (chemoattractant recep tor homologous molecule expressed on Th2)(1). EP receptor is subdivided into four subtypes, EP1, EP2, EP3, and EP4, on the basis of their responses to various agonists and antagonists.

Prostanoid receptors are G-protein coupled, rhodopsin type receptors with seven transmembrane domains. Knowl edge accumulated from analyses on the structure and func tion of the prostanoid receptor molecules has been de scribed elsewhere (2). The DP, EP2, EP4, IP receptors, and one isoform of the EP3 receptor can couple to G and thus increase intracellular cAMP concentration. The FP, IP, and TP receptors can couple to Gq, and activation of these re ceptors leads to an increase in intracellular calcium levels.