β2-Adrenergic receptor agonists, which act directly on smooth muscle in the airways causing dilation and increased air flow, are standard therapy for treating bronchospasm in asthmatics. Both short- and long-acting agonists are used in the management of asthma, although there are increasing concerns that chronic use of β2-agonists is associated with loss of disease control and may increase mortality in asthmatics. A study published in the journal PNAS has now shown that β2-adrenergic receptor inverse agonists reduce symptoms in an allergen-driven mouse model of asthma.
Although acute inhibition of β2-adrenergic receptor signalling narrows the airways, long term administration of a β2-inverse agonist caused similar improvements in asthma symptoms to genetic knock-out of the receptor. The researchers also found that chronic administration of alprenolol, a β-blocker without inverse agonist properties, did not reduce the symptoms, suggesting that basal signalling by empty receptors, rather than agonist-induced signalling, causes asthma. 
Whereas chronic exposure to β2-agonists leads to receptor down-regulation and worsening of asthma control, chronic blockade of the receptors may result in up-regulation and better control. Small scale clinical trials are being carried out to assess the effect of chronic dosing with the non-selective β-blocker, nadolol, in asthmatic patients.