Hindrance to gas flow in the bronchi is affected not only by airway smooth muscle tone but also by airway circulation. Congestion and oedema increase airway wall thickness and act in series with airway smooth muscle contraction to reduce airway calibre, an effect which is more marked in small and intermediate bronchi. Many mediators, neuromediators, paracrine mediators produced by resident (epithelium) or migrant (inflammatory cells) cells share bronchomotor and vascular effects. In addition, contraction of airway smooth muscle and vascular phenomena are mechanically coupled. Contraction of airway smooth muscle facilitates vascular congestion and oedema because the diameter of the muscle ring is more reduced than the external diameter of the airways. In addition, a negative intrathoracic pressure, e.g. in asthma, increases the mechanical loading of both ventricles, thereby facilitating pulmonary and bronchial oedema. The effects of this mechanical coupling are enhanced by airway inflammation that facilitates both vascular congestion and leakage. Stimuli such as exercise and hyperventilation cause airway vasodilatation which, in turn, facilitates and, possibly, triggers the post-exercise asthma attack. Conversely, congestion and vasodilatation may have a protective effect through an increase in the clearance of bronchoconstrictor substances, or in reducing the amplitude of airway cooling and water loss in exercise-induced asthma. The relative role in bronchial hyperresponsiveness of airway smooth muscle contraction and vascular phenomena probably depends upon individual factors such as, for instance, both intensity and nature of inflammation of the airway walls.