Prostanoids are the cyclooxygenase metabolites derived from C-20 unsaturated fatty acids (arachidonic acid). They include prostaglandin (PG) D2, PGE2, PGF2 alpha, PGI2, and thrombaxane (Tx) A2. The fatty acids precursors are released from the membrane phosphoplipids in response to various physiological and pathological stimuli by the action of phospholipase A2. They are converted to various prostanoids by the sequential actions of cyclooxygenases and the respective synthases. Prostaglandin PGE2 is one of the major prostaglandin produced during inflammation. A variety of PGE2- mediated effects on vascular smooth muscle tonus, glomerular cell function, renin release, and renal salt and water transport have been described. PGs also influence neuronal activity by modulating neurotransmitter release, sensitizing secretory fibers to noxious stimuli, or inducing fever and sleep. The actions of PGE2 are mediated by rhodopsin-type; G-protein coupled membrane receptors, termed E-prostanoid (EP) receptors or PTGERs. There are four subtypes of PGE receptors designated as EP1, EP2, EP3, and EP4. These receptors are encoded by different genes and expressed differently in each tissue. The intracellular signaling also differs among the receptor subtypes. In general, EP receptors display a protein topology typical of GPCR- 7 TM domain, an extracellular N-terminus, and a large intracellular C-terminus. EP1 expression is restricted to kidney (papillary collecting ducts), lung, and stomach (muscularis mucosae layer), spleen, skeletal muscle, testis, and uterus. EP1 has also been localized in neurons of the DRG. An alternatively spliced variant, a 366aa protein carrying a specific change if 49aa from the middle of TM VI to C-terminus, has also been described in rat uterus. The variant is also expressed in the kidney.