Endothelin-1 caused an increase in perfusion pressure, bronchial resistance, lung weight and tracheal effusion when infused through the pulmonary artery of rat and guinea-pig isolated lungs. In contrast to vasoconstriction, the effects of endothelin-1 on bronchial resistance, lung weight and tracheal effusion were not concentration-dependent. Recovery from vasoconstriction occurred within 15-30 min when the lung was further perfused with Krebs buffer. Increases in lung weight, bronchial resistance and tracheal effusion induced by endothelin-1 were irreversible when infused at concentrations above 10(-10) M. UK 38 485, a thromboxane A2 synthesis inhibitor, partly prevented the increase in lung weight and tracheal effusion without altering the vasoconstriction induced by endothelin-1. Such an antagonism was not seen in guinea-pig lung at the concentration used. Iloprost, a stable analogue of prostacyclin, antagonized the effects of endothelin-1 on perfusion pressure and lung weight without reducing tracheal effusion in both rat and guinea-pig lungs. Pretreatment with allopurinol did not alter the effects of endothelin-1. These results were taken as evidence for the potent lung oedema-producing effect of the peptide which seems to be partially mediated by the secondary release of thromboxane A2.