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Am J Physiol Lung Cell Mol Physiol (June 21, 2002). doi:10.1152/ajplung.00076.2002
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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.00076.2002
Submitted on March 11, 2002
Accepted on June 13, 2002

An endothelin receptor antagonist, SB217242 inhibits airways hyperresponsiveness in allergic mice

Peter J. Henry1*, Tracy S. Mann2, Angela C. D'Aprile2, Glenn J. Self2, and Roy G. Goldie1

1 Department of Pharmacology, University of Western Australia, Perth, Western Australia, Australia; Western Australian Institute for Medical Research, Nedlands, Western Australia, Australia
2 Department of Pharmacology, University of Western Australia, Perth, Western Australia, Australia

* To whom correspondence should be addressed. E-mail: phenry{at}receptor.pharm.uwa.edu.au.

Within the airways, endothelin-1 can exert a range of prominent effects including airway smooth muscle contraction, bronchial obstruction, airway wall edema, and airway remodeling. Endothelin-1 also possesses pro-inflammatory properties and contributes to the late phase response in allergic airways. However, there is currently no direct evidence for endogenous endothelin-1 contributing to airways hyperresponsiveness in allergic airways. Allergic inflammation induced in mice by sensitization and challenge with the house dust mite allergen Der P1 was associated with elevated levels of endothelin-1 within the lung, increased numbers of eosinophils within bronchoalveolar lavage fluid and tissue sections, and with the development of airways hyperresponsiveness to methacholine (p < 0.05, n = 6 mice per group). Treatment of allergic mice with an endothelin receptor antagonist SB 217242 (30 mg/kg/day) during allergen challenge, markedly inhibited airways eosinophilia (bronchoalveolar lavage fluid and tissue) and the development of airways hyperresponsiveness. These findings provide direct evidence for endothelin-1 playing a mediator role in the development of airways hyperresponsiveness and airways eosinophilia in Der P1-sensitized mice following antigen challenge.




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