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The Proceedings of the American Thoracic Society 5:23-31 (2008)
© 2008 The American Thoracic Society
doi: 10.1513/pats.200704-050VS

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Regulation of Airway Smooth Muscle Cell Contractility by Ca2+ Signaling and Sensitivity

Michael J. Sanderson1, Philippe Delmotte1, Yan Bai1 and Jose F. Perez-Zogbhi1

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

Correspondence and requests for reprints should be addressed to Michael J. Sanderson, Ph.D., Department of Physiology University of Massachusetts Medical School Worcester, MA. 01655. E-mail: michael.sanderson{at}umassmed.edu

ABSTRACT

Airway smooth muscle cell contraction is regulated by changes in intracellular Ca2+ concentration ([Ca2+]i) and the responsiveness of the airway smooth muscle cell to this Ca2+. The mechanism controlling [Ca2+]i primarily involves agonist-induced release of Ca2+ from internal stores to generate Ca2+ oscillations. The extent of contraction correlates with the persistence and frequency of these Ca2+ oscillations. The maintenance of the Ca2+ oscillations requires Ca2+ influx, but membrane depolarization appears to have a minor role in initiating or sustaining contraction. Contraction also requires agonist-induced Ca2+ sensitization, which is mediated mainly by decreases in myosin light-chain phosphatase activity. Although it is not clear if airway hyperresponsiveness associated with asthma results from the specific modulation of these Ca2+-based regulatory mechanisms, bronchodilators relax airways by both attenuating the Ca2+ oscillations and by decreasing the Ca2+ sensitivity.

Key Words: asthma • hyperresponsiveness • Ca2+ oscillations • relaxation




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