Although vagal reflexes are well documented in animal models of airway hyperresponsiveness, their importance in asthmatic attacks in man is less documented. Indeed most of the stimuli that can trigger bronchoconstriction act only partially through a cholinergic reflex. However, inflammatory mediators released in airways during asthma attacks may stimulate different sites of cholinergic pathways, i.e. in the sensory receptors, afferent, efferent, ganglionic or postganglionic sites. Further studies are required to assess the real influence of chemical mediators on vagal activity in asthmatic subjects during spontaneous or induced bronchoconstriction.