Abstract
In individuals with asthma, chronic use of short (SABAs) and long-acting beta-2 agonists (LABAs) can lead to loss of bronchoprotection (LOBP) from direct and indirect stimuli.1-3 It is hypothesized that LOBP is the result of beta-2 receptor down-regulation, reduced production or internalization of receptors, and uncoupling from secondary messengers leading to desensitization of beta-2 receptors.4 Assessment of beta-2 receptor activation is a laborious process.5 Therefore, a biomarker that serves as an indirect method of measuring beta-2 receptor activation would facilitate clinical studies on beta-2 agonist-induced LOBP and beta-2 receptor desensitization.
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