A neuronal cholinergic system is widely distributed in larger airways, particularly around bifurcations. These neurons form efferent pathways from the brainstem ending in the motor end-plate on smooth muscle, and ciliated and mucus-producing cells. Impulses originating in various sensory endings in the airways, from the central nervous system and from many sensory receptors throughout the body, influence the activity of the cholinergic system thereby controlling the patency of the airways and modulating the rate and depth of breathing. A non-neuronal cholinergic system present on mast cells facilitates their degranulation, resulting in the release of chemical mediators. These induce bronchospasm directly but also indirectly by activating the neuronal cholinergic system. Effective bonchodilator drugs are all antagonists of the cholinergic system. The most effective bronchodilators, however, are physiological antagonists of cholinergic and all other known bronchospasm-inducing agents. Such antagonists include beta-adrenergic stimulants and methyl xanthines. Competitive antagonists such as ipratropium which act on muscarinic receptors in the cholinergic motor end-plate are generally less effective. Drugs such as sodium cromoglycate act only prophylactically by reducing the degranulation of mast cells and/or minimizing irritation of airway sensory receptors.