Middleton E
J Allergy Clin Immunol. 1985 Aug;76(2 Pt 2):341-6. doi: 10.1016/0091-6749(85)90651-7.
Calcium ions participate in the pathogenesis of asthma. Increased cytosolic concentrations of free Ca2+ must develop to trigger smooth muscle contraction, mast cell mediator release, mucous gland secretion, vagal nerve activity, and the movement of inflammatory cells into the walls of the airways. Recent interest has centered on the possibility that Ca2+ antagonists might be useful in the treatment of asthma. Evidence now exists that airway smooth muscle contraction and mast cell and basophil mediator release may be inhibited by the calcium channel blockers nifedipine and verapamil. Other experiments indicate that these drugs may interfere with EIA and bronchoconstriction provoked by cold air and methacholine, for example. CaM antagonists may also interfere with smooth muscle contraction and mediator release. It is possible that more specific calcium antagonists, both Ca2+ channel blockers and CaM-active compounds, will be developed and find use as effective antiasthmatic agents.
钙离子参与哮喘的发病机制。必须使胞质内游离Ca2+浓度升高才能引发平滑肌收缩、肥大细胞介质释放、黏液腺分泌、迷走神经活动以及炎症细胞向气道壁的移动。最近人们的兴趣集中在Ca2+拮抗剂可能用于治疗哮喘这一可能性上。目前有证据表明，钙通道阻滞剂硝苯地平和维拉帕米可抑制气道平滑肌收缩以及肥大细胞和嗜碱性粒细胞介质释放。其他实验表明，例如这些药物可能会干扰冷空气和乙酰甲胆碱引发的迟发性哮喘反应（EIA）和支气管收缩。钙调蛋白拮抗剂也可能干扰平滑肌收缩和介质释放。有可能会研发出更具特异性的钙拮抗剂，包括Ca2+通道阻滞剂和具有钙调蛋白活性的化合物，并将其用作有效的抗哮喘药物。
