Ipratropium bromide potentiates bronchoconstriction induced by vagal nerve stimulation in the guinea-pig

Allison Fryer, Jennifer Maclagan

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)187-191
Number of pages5
JournalEuropean Journal of Pharmacology
Volume139
Issue number2
DOIs
StatePublished - Jul 9 1987
Externally publishedYes

Fingerprint

Ipratropium
Vagus Nerve Stimulation
Bronchoconstriction
Guinea Pigs
Muscarinic Receptors
Acetylcholine
Lung
Muscarinic Antagonists
Bronchodilator Agents
Bradycardia
Smooth Muscle
Pharmaceutical Preparations

Keywords

  • (Guinea-pig)
  • Bronchoconstriction (vagally induced)
  • Ipratropium

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology

Cite this

Ipratropium bromide potentiates bronchoconstriction induced by vagal nerve stimulation in the guinea-pig. / Fryer, Allison; Maclagan, Jennifer.

In: European Journal of Pharmacology, Vol. 139, No. 2, 09.07.1987, p. 187-191.

Research output: Contribution to journalArticle

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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.

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