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Am J Physiol Lung Cell Mol Physiol (June 21, 2002). doi:10.1152/ajplung.00084.2002
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Articles in PresS, published online ahead of print June 21, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00084.2002
Submitted on March 22, 2002
Accepted on June 12, 2002

Muscarinic M2 receptors in acetylcholine-isoproterenol functional antagonism in human isolated bronchus

BENJAMIN SARRIA1, EMMANUEL NALINE2, YONG ZHANG3, JULIO CORTIJO1, MATHIEU MOLIMARD2, JOELLE MOREAU2, PATRICE THEROND2, CHARLES ADVENIER2, and ESTEBAN J. MORCILLO1*

1 Departament de Farmacologia, universitat de Valencia. Facultat de Medicina i Odontologia, Valencia, Valencia, Spain
2 Departament de Farmacologia, Faculte de Medecine Paris-Ouest, UFR Biomedicale des Saint Peres and Centre Hospitalire de Versailles, Paris, Paris, France
3 Second Medical University of Shangai, Shangai, Shangai, China

* To whom correspondence should be addressed. E-mail: esteban.morcillo{at}uv.es.

The muscarinic functional antagonism of isoproterenol relaxation and the contribution of M2 receptors was examined in human isolated bronchus. In intact tissues, acetylcholine precontraction decreased isoproterenol potency and maximal relaxation (pD2 shift -1.49±0.16 and 30% Emax inhibition for 100µM acetylcholine) more than for same levels of histamine contraction. The M2 selective antagonist methoctramine (1µM) reduced this antagonism in acetylcholine but not histamine-contracted tissues. Similar results were obtained for forskolin-induced relaxation. After selective inactivation of M3 receptors with 4-DAMP mustard (30nM) demonstrated by abolition of contractile and inositol phosphate responses to acetylcholine, muscarinic recontractile responses were obtained in U46619 precontracted tissues fully relaxed with isoproterenol. Methoctramine antagonized recontraction with pKB (6.9) higher than in intact tissues (5.4) suggesting participation of M2 receptors. In M3 inactivated tissues, methoctramine augmented the isoproterenol relaxant potency in U46619 contracted bronchus, and reversed the acetylcholine-induced inhibition of isoproterenol cyclic AMP accumulation. These results indicate that M2 receptors cause indirect contraction of human bronchus by reversing sympathetically mediated relaxation and contribute to cholinergic functional antagonism.




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