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J Appl Physiol (May 30, 2003). doi:10.1152/japplphysiol.00272.2003
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Submitted on March 14, 2003
Accepted on May 16, 2003

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

Albrecht Bergner1 and Michael J Sanderson1*

1 Department of Physiology, University of Massachusetts Medical School, Worcester, MA, USA

* To whom correspondence should be addressed. E-mail: Michael.Sanderson{at}umassmed.edu.

To investigate the hypothesis that altered Ca2+ signaling in airway smooth muscle cells (SMCs) is responsible for airway hyper-reactivity we compared, with 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 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 hyper-reactivity in different mouse strains resides with the Ca2+ sensitivity of the contractile apparatus of the SMCs rather than with the Ca2+ signaling itself.




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