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Articles in PresS, published online ahead of print November 23, 2001
J Appl Physiol, 10.1152/jap.00934.2001
Submitted on September 10, 2001
Accepted on November 20, 2001
1 Medicine, Johns Hopkins School of Medicine, Baltimore, MD, USA
2 Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
3 Medicine, Johns Hopkins School of Medicine, Baltimore, MD, USA; Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: djacoby{at}jhmi.edu.
Viral infection causes dysfunction of inhibitory M2 muscarinic receptors (M2Rs) on parasympathetic nerves leading to airway hyperreactivity. The mechanisms of M2R dysfunction are incompletely understood. Double-stranded RNA (dsRNA), a product of viral replication, promotes the expression of interferons (IFNs). IFN
decreases M2R gene expression in cultured airway parasympathetic neurons. In this study, guinea pigs were treated with dsRNA (1 mg.kg-1i.p.) on two consecutive days. Twenty-four hours later anesthetized guinea pigs had dysfunctional M2Rs and were hyperresponsive to electrical stimulation of the vagus nerves, in the absence of inflammation. DsRNA did not affect either cholinesterase or the function of postjunctional M3Rs on smooth muscle. M2Rs on the nerves supplying the heart were also dysfunctional, but M2Rs on the heart muscle itself functioned normally. Thus, dsRNA causes increased bronchoconstriction and bradycardia via increased release of ACh from the vagus nerves due to loss of M2R function on parasympathetic nerves in the lungs and heart. Production of dsRNA may be a mechanism by which viruses cause dysfunction of neuronal M2Rs and airway hyperreactivity.
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