Asthma is characterized by bronchial hyperresponsiveness to a variety of bronchospasmogenic stimuli. To study the pathophysiologic mechanisms underlying the increased sensitivity and degree of maximal airway narrowing, various in vivo and in vitro models have been developed with methods of active and passive sensitization. These studies indicated a major role for alterations in the smooth muscle itself rather than neural dysfunction or airway inflammation as the underlying cause for the development of bronchial hyperresponsiveness. During the last years smooth muscle cells were found to exhibit not only the "classical" contractile phenotype but also a proliferative-synthetic phenotype, which is capable of producing proinflammatory cytokines, chemotaxins, and growth factors. Allergic sensitization can alter both contractile and secretory functions, thereby indicating that the smooth muscle cell could contribute directly to the persistence of airway inflammation in asthma. A better understanding of the changes within the smooth muscle cells and of the mechanisms that lead to their induction could contribute to the development of novel therapeutic approaches for the treatment of asthma.