TY - JOUR
T1 - Ipratropium bromide potentiates bronchoconstriction induced by vagal nerve stimulation in the guinea-pig
AU - Fryer, Allison D.
AU - Maclagan, Jennifer
N1 - Funding Information:
Financial support from Roche Products Limited is gratefully acknowledged.
PY - 1987/7/9
Y1 - 1987/7/9
N2 - In anaesthetised guinea-pigs, brinchoconstriction induced by vagal nerve stimulation was potentiated by low doses of the antimuscarinic bronchodilator drug, ipratropium (0.01-1.0 μg/kg); the maximum effect was obtained with 1.0 μg/kg which doubled the bronchoconstriction. When the dose was increased above 1.0 μg/kg potentiation no longer occured; instead the vagally induced bronchoconstriction was antagonised. This was accompanied by reduction in the bronchoconstriction and bradycardia induced by i.v. acetylcholine, due to blockade of post-junctional muscarinic receptors in the airways and heart. With 10 μg/kg ipratropium responses elicited both by vagal stimulation and by exogenous acetylcholine were abolished. The results show that ipratropium is an antagonist for pre-junctional muscarinic inhibitory receptors on pulmonary parasymphathetic nerves and also confirm its potent antagonist actions on post-junctional muscarinic receptors in the airway smooth muscle. The effect of ipratropium in the lung depends, therefore, on the balance the pre- and post-junctional effects.
AB - In anaesthetised guinea-pigs, brinchoconstriction induced by vagal nerve stimulation was potentiated by low doses of the antimuscarinic bronchodilator drug, ipratropium (0.01-1.0 μg/kg); the maximum effect was obtained with 1.0 μg/kg which doubled the bronchoconstriction. When the dose was increased above 1.0 μg/kg potentiation no longer occured; instead the vagally induced bronchoconstriction was antagonised. This was accompanied by reduction in the bronchoconstriction and bradycardia induced by i.v. acetylcholine, due to blockade of post-junctional muscarinic receptors in the airways and heart. With 10 μg/kg ipratropium responses elicited both by vagal stimulation and by exogenous acetylcholine were abolished. The results show that ipratropium is an antagonist for pre-junctional muscarinic inhibitory receptors on pulmonary parasymphathetic nerves and also confirm its potent antagonist actions on post-junctional muscarinic receptors in the airway smooth muscle. The effect of ipratropium in the lung depends, therefore, on the balance the pre- and post-junctional effects.
KW - (Guinea-pig)
KW - Bronchoconstriction (vagally induced)
KW - Ipratropium
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U2 - 10.1016/0014-2999(87)90251-2
DO - 10.1016/0014-2999(87)90251-2
M3 - Article
C2 - 2958300
AN - SCOPUS:0023237558
SN - 0014-2999
VL - 139
SP - 187
EP - 191
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
IS - 2
ER -