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Review
. 2003 Aug;112(4):495-7.
doi: 10.1172/JCI19642.

Beta-agonists and asthma: too much of a good thing?

Stephanie A Shore  1 , Jeffrey M Drazen
Affiliations
Review

Beta-agonists and asthma: too much of a good thing?

Stephanie A Shore et al. J Clin Invest. 2003 Aug.

Abstract

In an unusual paradox, asthmatics who are chronically treated with bronchodilating beta-agonists sometimes experience a worsening of their condition. A new study describes one possible mechanism and reveals a potential new therapeutic target in the treatment of asthma.

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Figures

Figure 1
Figure 1
(a) Mechanism of β-agonist–induced airway smooth muscle relaxation. Ligand binding to the β2AR activates Gs, leading to adenylyl cyclase (AC) activation, cAMP formation, and subsequent protein kinase A (PKA) activation. PKA phosphorylation of target proteins leads to smooth muscle relaxation and may also inhibit ERK activation. PKA also phosphorylates the β2AR, leading to increased Gi coupling. In addition, ligand binding causes G protein receptor kinase (GRK) phosphorylation of the β2AR, recruiting β-arrestin (ARR). (b) Inflammatory events in the asthmatic airway or regular β-agonist use may augment Gi coupling and/or increase β-arrestin binding. Under these circumstances, β-agonists may result in ERK activation, potentially amplifying production of inflammatory cytokines and leading to airway remodeling. Persistent activation of the β2AR may also lead to phospholipase C-β (PLCβ) expression and consequent airway hyperresponsiveness (8).
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