This chapter examines the evidence that one group of mediators, prostaglandins (PGD) and thromboxane (Tx), are involved in the pathogenesis of asthmatic responses. Most of the prostanoid receptors have been cloned and are found to belong to the family of G protein–coupled receptors with seven transmembrane domains. The bronchoconstrictive actions of TxA2, PGD2, and PGF2α are mediated by the thromboxane receptor (TP). The PGD D2 (DP) receptor is preferentially activated by PGD2, and it mediates vasodilation. EP receptors mediate the relaxation of airway smooth muscle (ASM) and inhibition of inflammatory cells in response to PGE2. The PGDs are categorized in two classes to evaluate their possible role in asthma: stimulatory PGDs—such as PGD2, PGF2α, and TxA2—which are potent bronchoconstrictors, and inhibitory PGDs, such as PGE2, which can reduce bronchoconstrictor responses and attenuate the release of acetylcholine from airway nerves.