Think the impossible: β-blockers for treating asthma

Abstract

Asthma was originally thought to be associated with an intrinsic defect in β2ADR (β2-adrenoceptor) function, tipping the balance towards parasympathetic bronchoconstriction. Hence β-blocking drugs (such as β2ADR antagonists and inverse agonists) may cause acute bronchoconstriction which, in turn, may be attenuated by anti-cholinergic agents. Although β2-agonists are highly effective for the acute relief of bronchoconstriction, their chronic use is accompanied by an adaptive reduction in β2ADR numbers and associated desensitization of response, resulting in increased exacerbations and rare cases of death. The hypothesis examined in the present article is that, while single dosing with a β-blocker may cause acute bronchoconstriction, chronic dosing may afford putative beneficial effects including attenuated airway hyper-responsiveness.