In anaesthetized guinea-pigs, gallamine produced a dose-related potentiation of the bronchoconstriction induced by electrical stimulation of the cervical vagus nerves; (+)-tubocurarine and suxamethonium lacked this effect. The bronchoconstriction produced by intravenous injection of acetylcholine or histamine, however, was not potentiated by gallamine. Vagally-induced bradycardia was abolished by gallamine, confirming antagonism of the effect of acetylcholine on muscarinic receptors in the heart. The muscarinic receptor agonist pilocarpine, had the opposite effect to gallamine in the lung as it inhibited vagally-mediated bronchoconstriction. Pretreatment of guinea-pigs with either guanethidine or propranolol did not affect the gallamine-induced potentiation of vagally-mediated bronchoconstriction. The potentiating effect of gallamine in the lung can be explained by blockade of inhibitory, muscarinic receptors located in the parasympathetic nerves supplying the lungs.