Asthma is defined as reversible airflow obstruction; the mechanism for this airflow obstruction is considered to be caused by a combination of an inflammatory process leading to a thickened edematous airway lining and bronchial smooth muscle constriction. The identification of specific beta-receptors in the autonomic system led to the development in the early 1960s of selective beta 2-agonists with their precise effects on the bronchial smooth muscle without direct action on cardiac muscle. The early beta 2-agonists such as salbutamol have a comparatively short bronchodilator action but a rapid onset of action, making them useful as "rescue" bronchodilators. Regular beta 2-agonists alone may mask the underlying pathogenesis of asthma and may be associated with tachyphylaxis or rebound bronchial hyperreactivity. The observation that a thickened airway lining may lead to disproportionate increases in airways resistance with small changes in bronchial muscle shortening suggests beta 2-agonists should be given in conjunction with anti-inflammatory therapy. With their long duration of action but slow onset the new beta 2-agonists may have a role in prophylaxis of asthma rather than rescue bronchodilation.