Sanderson, Michael J.Delmotte, PhilippeBai, YanPerez, Jose F.2022-08-232022-08-232007-12-212009-03-16Proc Am Thorac Soc. 2008 Jan 1;5(1):23-31. <a href="http://dx.doi.org/10.1513/pats.200704-050VS">Link to article on publisher's site</a>1546-3222 (Print)10.1513/pats.200704-050VS18094081https://hdl.handle.net/20.500.14038/38479Airway 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.en-USAnimalsAsthmaCalcium ChannelsCalcium SignalingHumansInositol 1,4,5-Trisphosphate ReceptorsMembrane PotentialsMuscle ContractionMuscle RelaxationMuscle, SmoothRyanodine Receptor Calcium Release ChannelLife SciencesMedicine and Health SciencesJournal Articlehttps://escholarship.umassmed.edu/oapubs/1351783032oapubs/1351