1 Electrical stimulation of the cervical vagi (15 Hz, 0.2 ms, 3s, 7-15 V) produced a slight bronchoconstriction in the anaesthetized guinea-pig. This effect was fully abolished by atropine, while gallamine (0.1-lOymol kg-1) produced a dose-dependent increase up to ten fold.2 Gallamine-induced potentiation of neurally-mediated bronchoconstriction was not inhibited by depletion of sensory neuropeptides with capsaicin or by pretreatment with pyrilamine. In propranololpretreated guinea-pigs the potentiation induced by gallamine 3 and 10 imol kg1 was inhibited by 40 and 46%, respectively. 3 Physostigmine (0.5 mg kg-1) produced a very slight and slowly developing bronchoconstriction in the anaesthetized guinea-pig, which was also potentiated dose-dependently by gallamine (0.1-10umol kg-1). 4 Gallamine (1 0 mol kg 1) potentiated the bronchial anaphylactic response induced by aerosol challenge with ovalbumin in actively sensitized guinea-pigs. 5 These results suggest that neither sensory neuropeptides nor histamine are involved in the gallamineinduced potentiation of neurally-mediated bronchoconstriction, while inhibition of the sympathetic nervous system may play a minor role. They are in general agreement with the hypothesis that gallamine antagonizes acetylcholine selectively at prejunctional muscarinic receptors in the guinea-pig airways, thus increasing its release from parasympathetic nerve terminals. These autoreceptors appear to be operant during anaphylactic bronchoconstriction.