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Airway Hyperresponsiveness: From Molecules to Bedside

Selected Contribution: Airway contractility and smooth muscle Ca²⁺ signaling in lung slices from different mouse strains

Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655

Submitted 14 March 2003 ; accepted in final form 16 May 2003

To investigate the hypothesis that altered Ca²⁺ signaling in airway smooth muscle cells (SMCs) is responsible for airway hyperreactivity, we compared, with the use of confocal and phase-contrast microscopy, the airway contractility and Ca²⁺ changes in SMCs induced by acetylcholine (ACh) in lung slices from different mouse strains (A/J, Balb/C, and C3H/ HeJ). The airways from each mouse strain displayed a concentration-dependent contraction to ACh. The contractile response of the airways of the C3H/HeJ mice was found, in contrast to earlier studies, to be much greater and faster than that of A/J and Balb/C mice. This difference in airway reactivity can be, in part, attributable to halothane, a volatile anesthetic that was previously used during in vivo measurements of airway reactivity but found here to significantly alter the ACh contractile response of airways in lung slices. The ACh-induced Ca²⁺ response of the airway SMCs in all of the various mouse strains was also concentration dependent. The magnitude of the initial Ca²⁺ increase and the frequency of the subsequent Ca²⁺ oscillations induced by ACh increased with ACh concentration. However, no differences in the Ca²⁺ responses to ACh could be distinguished between the mouse strains. These results suggest that the mechanism responsible for airway hyperreactivity in different mouse strains resides with the Ca²⁺ sensitivity of the contractile apparatus of the SMCs rather than with the Ca²⁺ signaling itself.

hyperreactivity; asthma; acetylcholine; halothane; confocal microscopy

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