Asthma is characterised by an excessive airway narrowing in response to a variety of stimuli, called airway hyperresponsiveness (AHR). Previous comparisons between mouse strains have shown that increased velocity of airway narrowing correlates with baseline airway responsiveness. These data prompted the investigation into models of induced AHR to see whether airway narrowing dynamics correlated with in vivo responsiveness.In an attempt to reproduce some of the features of asthma, BALB/c mice were sensitised and subjected to either brief or chronic periods of allergen exposure. Brief exposure involved two challenges with intranasal chicken egg ovalbumin (OVAin). Chronic exposure involved six 2-day periods of OVAin challenges, each separated by 12 days. Control mice received intranasal saline challenges. Outcomes included videomicrometry of lung slices (magnitude and velocity of airway narrowing), in vivo respiratory physiology measurements and histological staining with morphometric analysis.Neither brief nor chronic allergen exposure resulted in greater airway narrowing and increased velocity compared with saline controls. Structural changes in the airway, such as goblet cell hyperplasia, subepithelial fibrosis and increased contractile tissue, were detected in mice chronically challenged with allergen.In conclusion, increased responsiveness to methacholine following allergen challenge may not be due to an intrinsic change to the smooth muscle per se, but rather to other changes in the lung, which ultimately manifest as an increase in respiratory resistance.

The primary complaints from patients with asthma pertain to function of airway smooth muscle (ASM) function including shortness of breath, wheezing, and coughing. Thus, it is imperative to better understand the mechanisms underlying excitation-contraction coupling in ASM. Here, we review the various signaling pathways underlying contraction in ASM, and then examine how these are altered in asthma and airway hyperresponsiveness (a hallmark feature of asthma). Throughout, we highlight how studies of vascular smooth muscle have helped or hindered progress in understanding ASM physiology and pathophysiology.