Abstract:
:Membrane preparations of guinea-pig lung (containing multiple muscarinic receptor subtypes) and heart (containing M2 receptors only) were incubated with either neuraminidase, parainfluenza virus (which contains neuraminidase), or virus plus 2,3-dehydro-2-deoxy-N-acetylneuraminic acid, a neuraminidase inhibitor. None of these treatments affected [3H]quinuclidinyl benzilate [( 3H]QNB) binding. In the lung and heart, carbachol displaced 0.2 nM [3H]QNB from two sites. After treatment with either neuraminidase or virus the high affinity site was shifted to the right, and carbachol displaced QNB from one site with low affinity in the lung. In contrast, neuraminidase or virus decreased the affinity of carbachol for both sites in the heart. The neuraminidase inhibitor completely blocked virus-induced changes in carbachol affinity in both tissues. These results suggest that parainfluenza virus decreases the affinity of agonists for some of the muscarinic receptors in the lung, and for all of the muscarinic receptors in the heart due to its neuraminidase activity, which results in removal of sialic acid. The decreased agonist affinity in the lung may be responsible for the increased vagally induced bronchoconstriction seen in viral respiratory infections.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Fryer AD,el-Fakahany EE,Jacoby DBdoi
10.1016/0014-2999(90)90244-zsubject
Has Abstractpub_date
1990-05-31 00:00:00pages
51-8issue
1-2eissn
0014-2999issn
1879-0712pii
0014-2999(90)90244-Zjournal_volume
181pub_type
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journal_title:European journal of pharmacology
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journal_title:European journal of pharmacology
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