Abstract
Asthma was originally thought to be associated with an intrinsic defect in beta(2)ADR (beta(2)-adrenoceptor) function, tipping the balance towards parasympathetic bronchoconstriction. Hence beta-blocking drug!; (such as beta(2)ADR antagonists and inverse agonists) may cause acute bronchoconstriction which, in turn, may be attenuated by anti-cholinergic agents. Although beta(2)-agonists are highly effective for the acute relief of bronchoconstriction, their chronic use is accompanied by an adaptive reduction in beta(2)ADR 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 beta-blocker may cause acute bronchoconstriction, chronic dosing may afford putative beneficial effects including attenuated airway hyperresponsiveness.
Original language | English |
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Pages (from-to) | 115-120 |
Number of pages | 6 |
Journal | Clinical Science |
Volume | 118 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - Jan 2010 |
Keywords
- Adrenoceptor
- Airway hyper-responsiveness
- Asthma
- Beta-blocker
- Bronchoconstriction
- Heart failure
- Smooth muscle
- Hypertensive patients
- Murine model
- beta(2)-adrenoceptor
- Agonists
- Exacerbations
- Subsensitivity
- Metaanalysis
- Predisposes
- Antagonists