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Thorax 1998;53:613-618 ( July )

Occasional review

Pulmonary neuronal M₂ muscarinic receptor function in asthma and animal models of hyperreactivity

R W Costello,^a D B Jacoby,^c A D Fryer^b

^a Department of Medicine, University of Liverpool, Liverpool L69 3GA, UK, ^b Department of Environmental Health Sciences, School of Hygiene and Public Health, ^c Division of Pulmonary and Critical Care Medicine, ^d Johns Hopkins Asthma and Allergy Center, Johns Hopkins University, Baltimore, Maryland, USA

Correspondence to: Dr R W Costello.

The first 150 words of the full text of this article appear below.

	Introduction

The dominant innervation of the airway smooth muscle is mediated by parasympathetic fibres which are carried in the vagus nerves. Activation of these cholinergic nerves releases acetylcholine which binds to M₃ muscarinic receptors on the smooth muscle causing contraction.¹ Acetylcholine also feeds back onto neuronal M₂ muscarinic receptors located on the postganglionic cholinergic nerves. Stimulation of these receptors further limits acetylcholine release, so these M₂ muscarinic receptors act as autoreceptors.^2 3 Loss of function of these M₂ receptors, as occurs in some patients with asthma and in animal models of hyperreactivity, leads to an increase in vagally mediated hyperreactivity. In this review we shall discuss the mechanisms that may account for the loss of function of these neuronal M₂ muscarinic receptors.

	Innervation of the airways by parasympathetic nerves

The vagus nerves carry preganglionic nerve fibres from the vagal nuclei in the medulla to ganglia in the airways.⁴ These parasympathetic ganglia are interspersed irregularly along the posterior aspect of . . . [Full text of this article]

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