Abstract
For the past 20 years, the hypothesis that bronchial asthma represents an imbalance between deficient activity of the beta-adrenergic receptor pathway and/or enhanced activity of alpha-adrenergic/muscarinic cholinergic pathways in the regulation of airway smooth muscle has been a popular idea. Although some evidence supports this hypothesis, direct proof of its validity has been elusive. Concepts regarding the pathobiology of asthma have shifted from a focus on changes in smooth muscle per se to the prominent inflammatory nature of this disorder. We review some of the evolving information regarding the pathogenesis of this disorder and discuss how altered neurohormonal regulation of key inflammatory cells may contribute to the asthmatic condition.
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