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

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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