It is not necessary to have excessive shortening of smooth muscle to cause the disproportionate bronchial obstruction which is a characteristic of bronchial hyperresponsiveness (HRB). There are also no convincing arguments favouring increased contractility in vivo of airway smooth muscle in subjects having HRB in vivo. Excessive bronchial obstruction seems to be linked to factors increasing the effects of smooth muscle contraction: hypertrophy of smooth muscle, excessive thickening of the wall linked to pre-existing bronchial lesions, vasodilatation and acute parietal oedema caused by stimuli used to demonstrate HRB. Activation of effectors involved in HRB may be by direct through action on the post junctional receptors, indirect through local liberation of paracrine mediators, or stimulation of bronchial receptors causing a reflex increase in vagal tone. Various techniques have been used to cause HRB in man and in different of animal species. Whether the method employed damages the epithelium, causes an inflammatory infiltrate or interfere with the degradation of paracrine mediators, HRB is both transient and weak. Thus experimental HRB does not open pathways for the research into the cause of asthma. On the other hand these studies permit a better understanding of factors which aggravate human asthma. Even the causes of human HRB are poorly understood. The prevalence of HRB is greater than of asthma, there is no narrow correlation between the severity of asthma and the intensity of HRB and there are arguments in favour of the familial segregation of HRB. The question is posed, therefore, whether HRB is similar to atopy with a genetic factor determining the predisposition to the expression of asthma under the influence of environmental factors.