Document Detail

Neural mechanisms in asthma.
MedLine Citation:
PMID:  10849478     Owner:  NLM     Status:  MEDLINE    
Advances in the understanding of neural mechanisms in asthma may provide novel therapeutic approaches in the treatment of asthma. Excessive activity of cholinergic nerves may be important in asthma. Dysfunction of M2 muscarinic receptors in asthma may lead to excessive bronchoconstriction and mucus secretion and can be induced in animal models by a range of stimuli including allergen, viral infection, ozone, eosinophil products and cytokines. Cholinergic mechanisms may be especially important in certain types of patients and anticholinergic agents provide protection against bronchospasm due to psychogenic factors or beta2-blockers. Non-adrenergic non-cholinergic (NANC) mechanisms, both inhibitory (i-NANC) and excitatory (e-NANC), may play a significant role in the pathophysiology of asthma. The putative neurotransmitters, vasoactive interstinal polypeptide (VIP) and nitric oxide (NO), mediate neural bronchodilation in human airways. There does not appear to be a defect in the i-NANC system in moderate or severe asthma. e-NANC is mediated by the sensory neuropeptides substance P (SP) and the more potent bronchoconstrictor neurokinin A (NKA). Various studies suggest that the SP content of human airways is increased in asthma. Tachykinins are not only present in sensory nerves, but also are produced by inflammatory cells such as alveolar macrophages, dendritic cells, eosinophils, lymphocytes and neutrophils. They can be released into the airways by stimuli such as allergen and ozone. Evidence suggests that in addition to smooth muscle contraction, which is mediated mainly by NK2 receptors, tachykinins also cause mucus secretion, plasma extravasation and stimulate inflammatory and immune cells. These effects are mediated by NK1 receptors. Recent studies have shown that NK2 receptor antagonists such as saredutant partially inhibit NKA-induced bronchoconstriction in asthmatics. Thus, tachykinin receptor antagonists have potential as therapies for asthma.
G F Joos; P R Germonpré; R A Pauwels
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology     Volume:  30 Suppl 1     ISSN:  0954-7894     ISO Abbreviation:  Clin. Exp. Allergy     Publication Date:  2000 Jun 
Date Detail:
Created Date:  2000-06-27     Completed Date:  2000-06-27     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  8906443     Medline TA:  Clin Exp Allergy     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  60-5     Citation Subset:  IM    
Ghent University Hospital, Belgium.
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MeSH Terms
Asthma / physiopathology*
Bronchodilator Agents / pharmacology
Parasympathetic Nervous System / physiopathology*
Respiratory System / drug effects
Tachykinins / pharmacology
Reg. No./Substance:
0/Bronchodilator Agents; 0/Tachykinins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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