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Am J Physiol Lung Cell Mol Physiol (October 26, 2001). doi:10.1152/ajplung.00360.2001
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Articles in PresS, published online ahead of print October 24, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00360.2001
Submitted on September 10, 2001
Accepted on October 21, 2001

Adenosine A3 receptor-mediated potentiation of mucociliary transport and epithelial ciliary motility

Manako Taira1, Jun Tamaoki1*, Kazuyuki Nishimura1, Junko Nakata1, Mitsuko Kondo1, Hisashi Takemura1, and Atsushi Nagai1

1 First Department of Medicine, Tokyo Women's Medical University, Tokyo, Japan

* To whom correspondence should be addressed. E-mail: jtamaoki{at}chi.twmu.ac.jp.

To examine the effect of adenosine A3 receptor stimulation on airway mucociliary clearance, we measured transport of Evans blue dye in rabbit trachea in vivo and ciliary motility of epithelium by photoelectric method in vitro. Mucociliary transport was enhanced dose-dependently by the selective A3 agonist IB-MECA and to a lesser extent by the less-selective APNEA, whereas the A1 agonist CPA and the A2 agonist CGS21680 did not. The effect of IB-MECA was abolished by pretreatment with the selective A3 antagonist MRS1220, but not by the A1 antagonist DPCPX or the A2 antagonist DMPX. Epithelial ciliary beat frequency was increased by IB-MECA in a concentration-dependent manner, the maximal increase being 33%, and this effect was inhibited by MRS1220. The IB-MECA-induced ciliary stimulation was not altered by the cAMP antagonist Rp-cAMPS but greatly inhibited by Ca2+-free medium containing BAPTA-AM. Incubation with IB-MECA increased intracellular Ca2+ contents. Therefore, A3 agonist enhances airway mucociliary clearance probably through Ca2+-mediated stimulation of ciliary motility of airway epithelium.






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