On Ca<sup>2+</sup>sensitivity and the airways: not just any smooth muscle

Ward, Jeremy P. T.

doi:10.1183/09031936.06.00099406

Cited by 2 publications

(1 citation statement)

References 21 publications

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“…Although the mechanisms of Ca 21 sensitivity in airway SMCs are not yet fully characterized (59,60), there have been many studies that indicate that increased Ca 21 sensitization most often reflects decreased MLCP activity (61). Although a full review is beyond the scope of this article, there is evidence for two major pathways leading to decreased MLCP activity in airway SMCs.…”

Section: Ca 2+ Sensitivity Of Smcsmentioning

confidence: 99%

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

Sanderson

Delmotte²,

Bai³

et al. 2008

Proceedings of the American Thoracic Society

106

110

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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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Section: Ca 2+ Sensitivity Of Smcsmentioning

confidence: 99%