1. Four types of prostanoid receptor are present on pulmonary arterial vessels of man. Thromboxane (TP) receptors mediate constriction and are blocked by antagonists such as BAY u-3405, GR 32,191 and EP 169. Prostaglandin (PG) EP3 receptors also mediate constriction, the agonist potency ranking being SC 46,275 > sulprostone > misoprostol > or = PGE2; this action needs to be borne in mind when PGE analogues are used therapeutically. 2. Prostaglandin E2 causes relaxation in a few pulmonary artery preparations: an EP2 receptor may be involved. Prostacyclin, acting through i.p. receptors, consistently produces relaxation and studies are in progress to determine the contribution made by K(+)-channel opening. Agonist potencies of stable prostacyclin analogues and non-prostanoid prostacyclin mimetics, such as BMY 45,778 and the novel diphenylindole CU 23, on human pulmonary artery and platelets are well correlated. Interestingly, the non-prostanoid mimetics show persistent relaxant effects in vitro, which may be related to their high lipophilicities. 3. Prostacyclin and iloprost are being used to treat severe pulmonary hypertension; further study of the pharmacodynamic and pharmacokinetic properties of other i.p. receptor agonists could produce improved therapy.