Newer drugs in management. Calcium antagonists.
Ca2+ ions are critical to the functions of the various cells involved in the pathogenesis of asthma. Interest has developed regarding the potential use of Ca2+ antagonists in the management of asthma and allergic diseases. The information accumulated to date suggests that Ca2+ entry blockers may decrease airway smooth muscle responses to contractile agonists and may also reduce chemical mediator release from mast cells. Both processes would be expected to modify favorably the pathophysiology of asthma. This seems to have been demonstrated with the findings that certain Ca2+ entry blockers may inhibit exercise-induced bronchospasm and cold air- and antigen-induced airway narrowing. In several but not all experiments a direct bronchodilating effect of nifedipine was found in some subjects. In asthmatic patients with coexistent cardiovascular disease requiring beta-blocker therapy, it would be appropriate to use drugs such as the currently available Ca2+ entry blockers in place of the contraindicated beta-blocking agents. It appears that the currently available Ca2+ entry blockers have not provided a breakthrough class of therapeutic agents for the treatment of asthma. However, it seems highly likely that new Ca2+ antagonist drugs can be expected which will have greater specificity for airway smooth muscle and perhaps other cell types involved in the pathogenesis of asthma.
Middleton
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D000818:Animals; D001249:Asthma / Q000188:drug therapy* / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use*; D006168:Guinea Pigs; D006636:Histamine Release / Q000187:drug effects; D006801:Humans; D007473:Ion Channels / Q000187:drug effects; D008407:Mast Cells / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects; D009543:Nifedipine / Q000494:pharmacology; D051381:Rats
D002121:Calcium Channel Blockers; D007473:Ion Channels; D009543:Nifedipine; D002118:Calcium