Sanderson Michael J, Delmotte Philippe, Bai Yan, Perez-Zogbhi Jose F
Department of Physiology University of Massachusetts Medical School Worcester, MA 01655, USA.
Proc Am Thorac Soc. 2008 Jan 1;5(1):23-31. doi: 10.1513/pats.200704-050VS.
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.
气道平滑肌细胞收缩受细胞内钙离子浓度（[Ca2+]i）变化以及气道平滑肌细胞对该钙离子反应性的调节。控制[Ca2+]i的机制主要涉及激动剂诱导细胞内储存的钙离子释放，从而产生钙离子振荡。收缩程度与这些钙离子振荡的持续性和频率相关。钙离子振荡的维持需要钙离子内流，但膜去极化在启动或维持收缩中似乎作用较小。收缩还需要激动剂诱导的钙离子致敏，这主要由肌球蛋白轻链磷酸酶活性降低介导。虽然尚不清楚与哮喘相关的气道高反应性是否源于这些基于钙离子的调节机制的特定调节，但支气管扩张剂通过减弱钙离子振荡和降低钙离子敏感性来舒张气道。
