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Modulatory role of tachykinin NK₁ receptor in cholinergic contraction of mouse trachea

¹ Dept Respiratory Diseases, Ghent University Hospital, and ² Heymans Institute of Pharmacology, Ghent University, Faculty of Medicine, De Pintelaan, Ghent, Belgium

CORRESPONDENCE: K. De Swert, Dept Respiratory Diseases, Ghent University Hospital, De Pintelaan 185, B-9000, Ghent, Belgium. Fax: 32 92402341. E-mail: Katelijne.Deswert@rug.ac.be

Keywords: airway contraction, knockout mice, neuropeptides, substance P receptor, tachykinins

Received: January 31, 2002
Accepted August 5, 2002

This study was supported by the Concerted Research Initiative of Ghent University (GOA Project 98-6). K.G. Tournoy was supported by the Fund for Scientific Research Flanders. K.O. De Swert was supported by the Concerted Research Initiative of Ghent University (GOA Project 98-6).

The role of the NK₁ receptor in airway contraction induced by electrical field stimulation (EFS) was evaluated by comparing the response in NK₁ receptor knockout mice (NK₁R^–/–) with that of NK₁ receptor wild-type controls (WT).

A frequency/response curve on tracheas from NK₁R^–/– mice and NK₁R WT littermates was constructed. After incubation with [³H]choline, [³H]acetylcholine release upon EFS was measured by high-performance liquid chromatography and liquid scintillation counting. The effects of atropine (1x10^–6 M), tetrodotoxin (1x10^–6 M) and a specific NK₁R antagonist (SR140333, 1x10^–8 M) were studied, as well as the effects of substance P (1x10^–5 M) on precontracted tracheas.

Upon EFS, NK₁R^–/– mice had a significant lower trachea contractility than the NK₁R WT animals, accompanied with less [³H]acetylcholine release. Pretreatment with atropine or tetrodotoxin abolished the EFS-induced contraction in both strains. Pretreatment with the NK₁R antagonist SR140333 significantly reduced the contractility in the NK₁R WT but not in the NK₁R^–/– mice. Substance P caused a small contraction in both NK₁R WT and NK₁R^–/– mice. Substance P induced a relaxation in precontracted tracheas in NK₁R WT but not in NK₁R^–/– mice.

The data presented here provide direct evidence that the NK₁ receptor augments cholinergic neurotransmission in mouse trachea.

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