Isoproterenol and salbutamol caused relaxation of guinea-pig trachea, and generation of PGE2. The phenomenon appears to be specific for beta-adrenergic agonists since the relaxant activity induced by atropine, theophylline and papaverine was not associated with generation of prostaglandin-like material from tracheal smooth muscles. Indomethacin reduced only slightly the relaxation of the tracheal tissue induced by isoproterenol and salbutamol. The possibility is discussed that the increased arachidonic acid metabolism during trachea beta-adrenergic relaxation represents a metabolic event involving phospholipid methylation and membrane fluidity.