Premium
Neuronal muscarinic receptors attenuate vagally‐induced contraction of feline bronchial smooth muscle
Author(s) -
Blaber L.C.,
Fryer Allison D.,
Maclagan Jennifer
Publication year - 1985
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1985.tb08951.x
Subject(s) - muscarinic acetylcholine receptor , contraction (grammar) , muscle contraction , muscarinic acetylcholine receptor m2 , receptor , atropine , cats , acetylcholine , smooth muscle , medicine , endocrinology , neuroscience , anatomy , chemistry , biology
1 In anaesthetized cats, stimulation of the vagus nerves produced bradycardia and a bronchoconstriction which was measured as an increase in lung resistance (R L ) and a fall in dynamic lung compliance (C dyn ); these effects were abolished by atropine. 2 Gallamine potentiated vagally‐mediated changes in R L and C dyn at doses that blocked muscarinic receptors in the heart and inhibited neuromuscular transmission. (+)‐Tubocurarine and suxamethonium did not affect the response of the lung or the heart to vagal stimulation. 3 Bronchoconstriction induced by intravenous acetylcholine was not potentiated by gallamine, indicating that postsynaptic muscarinic receptors in the lung and changes in muscle tone were not involved. 4 Potentiation of vagally‐induced bronchoconstriction appears to be due to blockade of inhibitory muscarinic receptors located in the pulmonary parasympathetic nerves innervating both central and peripheral airways. 5 Pilocarpine was an agonist for these neuronal receptors as it inhibited vagally‐induced bronchoconstriction at low doses (10 ng to 1 μg kg −1 ). 6 The results demonstrate that gallamine is an antagonist and pilocarpine an agonist at neuronal muscarinic receptors which attenuate parasympathetic nerve activity in feline lung.