Airway smooth muscle is under neurogenic and myogenic control and thus bronchial hyperresponsiveness in asthma may be related to an abnormality in one or other of these systems. Possible neurogenic mechanisms leading to hyperresponsiveness include an abnormality of vagal pathways, of alpha and beta adrenergic receptors in airway smooth muscle or of nonadrenergic noncholinergic nerves. The relative importance of these different mechanisms remains controversial, and regarding nonadrenergic noncholinergic pathway untested. The findings of some recent studies suggest that neither an alteration in vagal pathways nor of adrenergic receptors can be considered as the primary disorder accounting for nonspecific increases in bronchial responsiveness. Possible myogenic mechanisms for hyperresponsiveness include an increase in contractility of individual muscle cells or an increase in cell to cell coupling between muscle cells i.e. a shift from multi-unit to single unit behaviour. These hypotheses have only started to be tested experimentally.