Bronchial hyperresponsiveness is one of the main features of asthma. We previously reported that 1,1-dimethylphenyl1-4piperazinium (DMPP), a nicotinic receptor agonist, has an inhibitory effect on airway response to methacholine in an in vivo model of asthma. The aims of this study were to: a) verify if nicotinic acetylcholine receptors (nAchr) were present on mouse tracheal smooth muscle, b) if bronchoprotection observed in mice was due to a direct effect on airway smooth muscle, and, c) compare the effect of nicotinic agonists to that of salbutamol. Alpha-3, -4 and -7 nicotinic acetylcholine receptor subunits were detected by immunofluorescence on tracheal tissues from normal BALB/c mice. The effect of DMPP on tracheal responsiveness was verified by an isometric method. Tracheas were isolated from normal mice, placed in organ baths, and contracted with a single dose of methacholine. Cumulative doses of DMPP or salbutamol were added to the baths. Results show that mouse tracheal smooth muscle is positive for alpha-4 and -7 nAchr subunits, while the epithelium is positive for alpha-3, -4 and -7 subunits. DMPP induced a greater dose dependant relaxation of tracheal smooth muscles pre-contracted with methacholine than salbutamol. These results suggest that the smooth muscle relaxing effect of DMPP could have some interest in the treatment of obstructive pulmonary diseases.