Effects of tachykinin NK1 receptor antagonists on vagal hyperreactivity and neuronal M2 muscarinic receptor function in antigen challenged guinea-pigs

British Journal of Pharmacology
Richard W CostelloD B Jacoby

Abstract

1. The role of tachykinin NK1 receptors in the recruitment of eosinophils to airway nerves, loss of inhibitory neuronal M2 muscarinic receptor function and the development of vagal hyperreactivity was tested in antigen-challenged guinea-pigs. 2. In anaesthetized guinea-pigs, the muscarinic agonist, pilocarpine (1-100 microg kg(-1), i.v.), inhibited vagally induced bronchoconstriction, in control, but not in antigen-challenged guinea-pigs 24 h after antigen challenge. This indicates normal function of neuronal M2 muscarinic receptors in controls and loss of neuronal M2 receptor function in challenged guinea-pigs. Pretreatment of sensitized guinea-pigs with the NK1 receptor antagonists CP99994 (4 mg kg(-1), i.p.), SR140333 (1 mg kg(-1), s.c.) or CP96345 (15 mg kg(-1), i.p.) before antigen challenge, prevented M2 receptor dysfunction. 3. Neither administration of the NK1 antagonists after antigen challenge, nor pretreatment with an NK2 receptor antagonist, MEN10376 (5 micromol kg(-1), i.p.), before antigen challenge, prevented M2 receptor dysfunction. 4. Electrical stimulation of the vagus nerves caused a frequency-dependent (2-15 Hz, 10 V, 0.2 ms for 5 s) bronchoconstriction that was significantly increased following antigen chal...Continue Reading

References

Jul 1, 1990·British Journal of Pharmacology·S BrunelleschiR Fantozzi
Dec 1, 1991·Journal of Applied Physiology·A D Fryer, M Wills-Karp
Jan 1, 1987·Annals of the New York Academy of Sciences·C De SimoneF Sorice
Dec 1, 1989·Journal of Applied Physiology·P A MinetteP J Barnes
Apr 1, 1987·Naunyn-Schmiedeberg's Archives of Pharmacology·A D Fryer, J Maclagan
Dec 1, 1984·British Journal of Pharmacology·A D Fryer, J Maclagan
Sep 1, 1995·American Journal of Respiratory and Critical Care Medicine·H J PatelM G Belvisi
Jan 1, 1993·Acta Haematologica·F J WiedermannC J Wiedermann
Oct 1, 1993·The American Review of Respiratory Disease·C BertrandP Geppetti
Mar 28, 1996·European Journal of Pharmacology·M MalcangioM Perretti
May 1, 1996·Immunological Investigations·A E El-ShazlyT Ishikawa

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Citations

Oct 10, 2009·Current Allergy and Asthma Reports·Kirsten C VerheinDavid B Jacoby
Nov 20, 2001·Current Opinion in Pharmacology·G F Joos, R A Pauwels
May 24, 2001·American Journal of Respiratory and Critical Care Medicine·C M EvansA D Fryer
Jun 5, 2003·Expert Opinion on Therapeutic Targets·Alessandro Lecci, Carlo Alberto Maggi
Jun 13, 2014·Current Opinion in Pharmacology·Nastasia V WasilewskiJohn T Fisher
Sep 26, 2003·Psychosomatic Medicine·Ricarda A JoachimBurghard F Klapp
Apr 10, 2002·Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology·B D'AgostinoF Rossi
Apr 11, 2018·Journal of Leukocyte Biology·Matthew G DrakeZhenying Nie
Mar 22, 2003·The Journal of Pharmacology and Experimental Therapeutics·Renate BangGisa Tiegs
Feb 11, 2020·Journal of Leukocyte Biology·Katie M LeboldMatthew G Drake
Aug 17, 2002·Journal of Applied Physiology·Fernanda D T Q S LopesMilton A Martins
Jul 13, 2000·American Journal of Physiology. Lung Cellular and Molecular Physiology·D B JacobyA D Fryer
Nov 18, 2003·The Journal of Pharmacology and Experimental Therapeutics·Renate BangGisa Tiegs
Aug 25, 2000·American Journal of Physiology. Lung Cellular and Molecular Physiology·C M EvansA D Fryer

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