Of the five cloned muscarinic receptor subtypes, human airways express only three receptor subtypes (M1, M2 and M3) and these subtypes are differentially distributed in the airways [1]. M1-receptors are localised to alveolar walls, parasympathetic ganglia and submucosal glands, whereas M3-receptors are predominant in airway smooth muscle and submucosal glands. In contrast, M2-receptors are localised to airway smooth muscle of small airways, although there is little evidence that these receptors play an important functional role in the regulation of airway smooth muscle tone, at least in human airways. Functional studies suggest that M2-receptors play an important role in regulating the release of acetylcholine from parasympathetic nerves in the airways. M2-receptors which inhibit cholinergic neural contraction have been demonstrated in functional studies of human airways in vitro and pre-junctional M2-receptors inhibit the release of acetylcholine in animal and human airways [2,4]. There is considerable evidence that M2-receptors may be dysfunctional in patients with asthma and this might contribute to exaggerated cholinergic reflex bronchoconstriction in asthma [4]. There are several possible mechanisms that might result in dysfunction of M2-receptors, including viral infections, eosinophil basic proteins and oxidants. The inflammatory process may also result in impaired function of M2-receptors.