Calcium antagonists and asthma.
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.
Middleton
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D001249:Asthma / Q000503:physiopathology*; D001491:Basophils / Q000187:drug effects; D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use*; D002147:Calmodulin / Q000037:antagonists & inhibitors*; D006636:Histamine Release / Q000187:drug effects; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D007473:Ion Channels / Q000502:physiology; D008407:Mast Cells / Q000187:drug effects; D009130:Muscle, Smooth / Q000502:physiology
D002121:Calcium Channel Blockers; D002147:Calmodulin; D007473:Ion Channels; D002118:Calcium