Acetylcholine-induced bronchoconstriction modified by noise exposure in normal but not in sensitized guinea-pigs

1 The acute (6 h) exposure of guinea-pigs to white noise (110 dB) as a stress stimulus, reduced bronchial reactivity to acetylcholine (Ach) (3 - 1000 mu g kg(-1) i.v.) in anaesthetized animals. 2 The hyporesponsiveness to Ach in stressed animals was not confirmed in vitro on tracheal preparations (Ach 1x10(-9)-1x10(-4)g ml(-1)) and disappeared in vivo when the animals were sensitized with ovalbumin (OA, 100 mg kg(-1) i.p.+100 mg kg(-1) s.c.). The hyporesponsiveness was also absent in ovalbumin sensitized guinea-pigs exposed to an aerosol of ovalbumin 60 min before testing with Ach. 3 In non-sensitized guinea-pigs, pretreatment with butoxamine (1 mg kg(-1)i.v.) or with theophylline (25 mg kg(-1) i.v.), completely abolished the effect of noise-exposure. In contrast, pretreatment with L-N-G-nitro-arginine methyl ester (L-NAME, 10 mg kg(-1) i.v.), alpha-chymotrypsin (2 U kg(-1) i.v.) or with enprofylline (10 mg kg(-1) i.v.), did not affect it. 4 In conclusion, our experiments reveal inhibitory mechanisms upon Ach-induced bronchoconstriction activated by a stress stimulus and this is absent in sensitized animals. These mechanisms seem to be linked to the adrenergic beta 2-receptors and a role for the purinergic system (via A-receptors) may also be present.