In asthma, the administration (inhalation) of a selective β2 receptor agonist (e.g. salbutamol), prior to methacholine challenge has been shown to shift the dose response curve to the right and "bronchoprotect" the airway against airway smooth muscle contraction. The extent of β2 receptor agonist bronchoprotection in COPD is unknown.
Airway hyperresponsiveness (AHR) to direct acting agents such as histamine and methacholine is a feature of both asthma and COPD. In asthma, the abnormality leading to AHR is believed to be due to changes in airway smooth muscle (e.g. hypertrophy, hyperplasia, contractile apparatus) whereas in COPD the AHR is likely due to structural or geometric changes.
The investigators hypothesize that the bronchoprotection afforded by salbutamol against methacholine challenge will be greater in asthma than in COPD due to differences in underlying airway abnormalities.