This review summarizes recent data on the two specific mechanisms of beta-adrenergic relaxation of airway smooth muscle. Beta 2-adrenergic receptor stimulation results in the opening of large-conductance, calcium-activated potassium channels, and an attendant hyperpolarization of the myocyte. Coupling between receptor and channel occurs by phosphorylation-dependent and phosphorylation-independent mechanisms. Inhibition of channel opening by specific peptidyl toxins results in a shift in the dose-dependent relaxation of this tissue by beta-adrenergic hormones. There is also evidence that beta-adrenergic hormones can decrease the calcium sensitivity of contractile elements. This desensitization does not result from the phosphorylation of myosin light chain kinase but may be associated with the activation of a myosin light chain phosphatase.