Muscarinic acetylcholine receptors and airway diseases

Coulson, Fiona R. and Fryer, Allison D. (2003) Muscarinic acetylcholine receptors and airway diseases. Pharmacology & Therapeutics, 98 1: 59-69. doi:10.1016/S0163-7258(03)00004-4

Author Coulson, Fiona R.
Fryer, Allison D.
Title Muscarinic acetylcholine receptors and airway diseases
Journal name Pharmacology & Therapeutics   Check publisher's open access policy
ISSN 0163-7258
Publication date 2003-04
Sub-type Article (original research)
DOI 10.1016/S0163-7258(03)00004-4
Volume 98
Issue 1
Start page 59
End page 69
Total pages 11
Editor J. Wess
Place of publication London, UK
Publisher Elsevier Science
Language eng
Subject 11 Medical and Health Sciences
Formatted abstract
Parasympathetic nerves provide the dominant autonomic innervation of the airways. Release of acetylcholine from parasympathetic nerves activates postjunctional muscarinic receptors present on airway smooth muscle, submucosal glands, and blood vessels to cause bronchoconstriction, mucus secretion, and vasodilatation, respectively. Acetylcholine also feeds back onto prejunctional muscarinic receptors to enhance or inhibit further acetylcholine release. In asthma and chronic obstructive pulmonary disease, bronchoconstriction and mucus secretion is increased and the airways are hyperresponsive to contractile agents. These changes are due to increased parasympathetic nerve activity. The number and function of postjunctional muscarinic receptors in the airways are unchanged in animal models of asthma. Rather, it is the supply of acetylcholine to the postjunctional cells (smooth muscle and submucosal gland) that is increased. The increase in acetylcholine release occurs because prejunctional, inhibitory M2 muscarinic receptors on the parasympathetic nerves are dysfunctional. M2 muscarinic receptor dysfunction and subsequent airway hyperreactivity have been demonstrated to occur in animals in response to a variety of triggers, including antigen challenge, virus infection, ozone exposure, and vitamin A deficiency. In humans, there is evidence that loss of M2 muscarinic receptor function is related to asthma. The mechanisms by which neuronal M2 muscarinic receptor function is lost and its relevance to human airway disease are discussed in this review.
Keyword Prejunctional receptors
Postjunctional receptors
Parasympathetic nerves
Airway hyperreactivity
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
School of Medicine Publications
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Citation counts: TR Web of Science Citation Count  Cited 109 times in Thomson Reuters Web of Science Article | Citations
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Created: Tue, 11 Apr 2006, 01:57:52 EST