Asthma is a chronic disease characterized by intermittent episodes in which airway smooth muscle contracts strongly, markedly increasing airway resistance. The basic defect in asthma is chronic inflammation of the airways, the causes of which vary from person to person and include, among others, allergy, viral infections, and sensitivity to environmental factors. The important point is that the underlying inflammation causes the airway smooth muscle to be hyperresponsive and to contract strongly when, depending upon the individual, the person exercises (especially in cold, dry air) or is exposed to cigarette smoke, environmental pollutants, viruses, allergens, normally released bronchoconstrictor chemicals, and a variety of other potential triggers. In fact, the incidence of asthma is increasing, possibly due in part to environmental pollution.
The therapy for asthma is twofold: (1) to reduce the chronic inflammation and hence the airway hyperresponsiveness with so-called anti-inflammatory drugs, particularly inhaled glucocorticoids and leukotriene inhibitors, and (2) to overcome acute excessive airway smooth muscle contraction with bronchodilator drugs—that is, drugs that relax the airways. The latter drugs work on the airways either by relaxing airway smooth muscle or by blocking the actions of bronchoconstrictors. For example, one class of bronchodilator drug mimics the normal action of epinephrine on beta-adrenergic (beta-2) receptors. Another class of inhaled drugs are used to block muscarinic cholinergic receptors, which have been implicated in bronchoconstriction.