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

Eur J Pharmacol. 1987 Jul 9;139(2):187-91. doi: 10.1016/0014-2999(87)90251-2.


In anaesthetised guinea-pigs, bronchoconstriction induced by vagal nerve stimulation was potentiated by low doses of the antimuscarinic bronchodilator drug, ipratropium (0.01-1.0 microgram/kg); the maximum effect was obtained with 1.0 microgram/kg which doubled the bronchoconstriction. When the dose was increased above 1.0 microgram/kg potentiation no longer occurred; 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 micrograms/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 parasympathetic 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 between the pre- and post-junctional effects.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Atropine Derivatives / pharmacology*
  • Bronchi / drug effects*
  • Constriction, Pathologic
  • Drug Synergism
  • Electric Stimulation
  • Guinea Pigs
  • Ipratropium / pharmacology*
  • Muscle Contraction / drug effects
  • Muscle, Smooth / drug effects*
  • Vagus Nerve / physiology*


  • Atropine Derivatives
  • Ipratropium