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Am J Physiol Lung Cell Mol Physiol 279: L59-L65, 2000;
1040-0605/00 $5.00
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Vol. 279, Issue 1, L59-L65, July 2000

Effects of neurokinin receptor antagonists in virus-infected airways

David B. Jacoby1,2, Bethany L. Yost1, Thomas Elwood3, and Allison D. Fryer1

1 Department of Environmental Health Sciences, School of Hygiene and Public Health, and 2 Division of Pulmonary and Critical Care Medicine, Johns Hopkins Asthma and Allergy Center, Johns Hopkins University, Baltimore, Maryland 21224; and 3 Department of Anesthesiology, Children's Hospital and Medical Center, University of Washington, Seattle, Washington 95155

We investigated the effects of a neurokinin-1 (NK1) receptor antagonist (SR-140333) and a NK2 receptor antagonist (SR-48968) on airway responsiveness and on the function of neuronal M2 muscarinic receptors, which normally inhibit vagal acetylcholine release, in guinea pigs infected with parainfluenza virus. Antagonists were given 1 h before infection and daily thereafter. Four days later, bronchoconstriction induced by either intravenous histamine (which is partly vagally mediated) or electrical stimulation of the vagus nerves was increased by viral infection compared with control. In addition, the ability of the muscarinic agonist pilocarpine to inhibit vagally induced bronchoconstriction was lost in virus-infected animals, demonstrating loss of neuronal M2 receptor function. Macrophage influx into the lungs was inhibited by pretreatment with both antagonists. However, only the NK1 receptor antagonist prevented M2 receptor dysfunction and inhibited hyperresponsiveness (measured as an increase in either vagally induced or histamine-induced bronchoconstriction). Thus virus-induced M2 receptor dysfunction and hyperresponsiveness are prevented by a NK1 receptor antagonist, but not by a NK2 receptor antagonist, whereas both antagonists had similar anti-inflammatory effects.

virus; parasympathetic nerves; vagus nerves; asthma; histamine


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