Regulation of airway smooth muscle cell contractility by Ca2+ signaling and sensitivity
Department of Physiology; University of Massachusetts Medical School Worcester
Animals; Asthma; Calcium Channels; Calcium Signaling; Humans; Inositol 1,4,5-Trisphosphate Receptors; Membrane Potentials; Muscle Contraction; Muscle Relaxation; Muscle, Smooth; Ryanodine Receptor Calcium Release Channel
Life Sciences | Medicine and Health Sciences
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.
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Citation: Proc Am Thorac Soc. 2008 Jan 1;5(1):23-31. Link to article on publisher's site
DOI of Published Version
Proceedings of the American Thoracic Society
Sanderson, Michael J.; Delmotte, Philippe; Bai, Yan; and Perez, Jose F., "Regulation of airway smooth muscle cell contractility by Ca2+ signaling and sensitivity" (2007). Open Access Articles. 1351.