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Airway Receptors and Asthma

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Airway caliber is determined by a balance between many constrictor and dilator agents, which bring about their effects on the various target cells of the airway by activating specific cell surface receptors. Asthma and bronchial hyperresponsiveness may be viewed as an imbalance between excitatory and inhibitory receptor-mediated effects on the various target cells in the airway. Airway receptors can be grouped into those mediating the effects of the autonomic nervous system on the airways or those mediating the effects of the various mediators which may be generated in asthma. There is no convincing evidence that a fundamental defect in receptor function is involved in the pathogenesis of asthma, although minor abnormalities have been described. Recently there has been a considerable increase in our understanding of receptor function and control, which should throw light on the pathogenesis of airway obstruction and may lead to advances in asthma therapy. This may also lead to the development of novel drugs for treating asthma in the future.

Document Type: Research Article


Publication date: May 1, 1986

More about this publication?
  • Allergy and Asthma Proceedings is a peer reviewed publication dedicated to distributing timely scientific research regarding advancements in the knowledge and practice of allergy, asthma and immunology. Its primary readership consists of allergists and pulmonologists.

    The goal of the Proceedings is to publish articles with a predominantly clinical focus which directly impact quality of care for patients with allergic disease and asthma.

    Featured topics include asthma, rhinitis, sinusitis, food allergies, allergic skin diseases, diagnostic techniques, allergens, and treatment modalities. Published material includes peer-reviewed original research, clinical trials and review articles.

    Articles marked "F" offer free full text for personal noncommercial use only.

    The journal is indexed in Thomson Reuters Web of Science and Science Citation Index Expanded, plus the National Library of Medicine's PubMed service.
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