Bronchodilator therapy remains an essential complementary treatment of asthma. β2-agonists are the most effective currently available bronchodilators. They are effective both in relieving acute asthma symptoms and providing sustained bronchodilatation. They produce airway smooth muscle relaxation through β2-adrenoreceptor activation.  The structure, airway wall distribution and function of the receptor has been well known. However molecular mechanisms leading to airway smooth muscle relaxation are not fully understood. Β2-receptor activation increases levels of intracellular cyclic adenosine monophosphate (cAMP) through the stimulation of adenylyl cyclase and then subsequent activation of the cAMP-dependent protein kinase cascade. Protein kinase A is thought to be direct involved in the control of muscle tone by inducing the phosphorylation of muscle regulatory proteins and modification of cellular Ca2+ concentration. The cAMP-independent signaling pathways leading to airway muscle relaxation have also been described.

In this article, the current status of β2-receptor activation in the airways is reviewed. The molecular mechanisms of β2–receptor activation and smooth muscle cell relaxation has been described. The authors also present the current knowledge on the structure and function of β2-adrenoreceptor.