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    Acetylcholine-induced calcium signaling and contraction of airway smooth muscle cells in lung slices

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    Authors
    Bergner, Albrecht
    Sanderson, Michael J.
    UMass Chan Affiliations
    Department of Physiology
    Document Type
    Journal Article
    Publication Date
    2002-01-30
    Keywords
    Acetylcholine
    Animals
    Calcium Signaling
    Dose-Response Relationship, Drug
    Lung
    Male
    Mice
    Mice, Inbred BALB C
    Muscle Contraction
    Muscle, Smooth
    Physiology
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    Abstract
    The Ca(2+) signaling and contractility of airway smooth muscle cells (SMCs) were investigated with confocal microscopy in murine lung slices (approximately 75-microm thick) that maintained the in situ organization of the airways and the contractility of the SMCs for at least 5 d. 10--500 nM acetylcholine (ACH) induced a contraction of the airway lumen and a transient increase in [Ca(2+)](i) in individual SMCs that subsequently declined to initiate multiple intracellular Ca(2+) oscillations. These Ca(2+) oscillations spread as Ca(2+) waves through the SMCs at approximately 48 microm/s. The magnitude of the airway contraction, the initial Ca(2+) transient, and the frequency of the subsequent Ca(2+) oscillations were all concentration-dependent. In a Ca(2+)-free solution, ACH induced a similar Ca(2+) response, except that the Ca(2+) oscillations ceased after 1--1.5 min. Incubation with thapsigargin, xestospongin, or ryanodine inhibited the ACH-induced Ca(2+) signaling. A comparison of airway contraction with the ACH-induced Ca(2+) response of the SMCs revealed that the onset of airway contraction correlated with the initial Ca(2+) transient, and that sustained airway contraction correlated with the occurrence of the Ca(2+) oscillations. Buffering intracellular Ca(2+) with BAPTA prohibited Ca(2+) signaling and airway contraction, indicating a Ca(2+)-dependent pathway. Cessation of the Ca(2+) oscillations, induced by ACH-esterase, halothane, or the absence of extracellular Ca(2+) resulted in a relaxation of the airway. The concentration dependence of the airway contraction matched the concentration dependence of the increased frequency of the Ca(2+) oscillations. These results indicate that Ca(2+) oscillations, induced by ACH in murine bronchial SMCs, are generated by Ca(2+) release from the SR involving IP(3)- and ryanodine receptors, and are required to maintain airway contraction.
    Source
    J Gen Physiol. 2002 Feb;119(2):187-98.
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/38183
    PubMed ID
    11815668
    Related Resources
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    UMass Chan Faculty and Researcher Publications

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