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Experimental Physiology 90.4 pp 535-544
DOI: 10.1113/expphysiol.2004.028746
© The Physiological Society 2005
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ATP regulation of ciliary beat frequency in rat tracheal and distal airway epithelium

Tetsuya Hayashi1, Manpei Kawakami1, Shinjiro Sasaki1, Takahiro Katsumata1, Hiroshi Mori2, Hideyo Yoshida3 and Takashi Nakahari3

1 Department of Thoracic and Cardiovascular Surgery2 Department of Pathology3 Department of Physiology, Osaka Medical College, Takatsuki, Osaka 569-8686, Japan

Ciliary beat frequency (CBF) was measured by video-optical microscopy in rat tracheal and distal airway ciliary cells using a slice preparation. In tracheal ciliary cells (tracheal slice), ATP or 2-methylthio ATP (MeSATP) increased CBF, which was inhibited by suramin (100 µM, an inhibitor of purinergic receptor). Ionomycin (5 µM) or thapsigargin (2 µM) increased CBF similarly. Ca2+-free solution or addition of Ni2+ (1 mM) decreased CBF gradually by approximately 25% and subsequent stimulation with ATP (10 µM) increased CBF transiently. The purinergic agonist experiments demonstrated that ATP increases CBF in tracheal ciliary cells via both P2X and P2Y receptors. ATP increased the intracellular calcium concentration ([Ca2+]i) in tracheal ciliary cells. However, in distal airway ciliary cells (lung slice), ATP did not increase CBF and [Ca2+]i, although a Ca2+-free solution decreased CBF, and ionomycin (5 µM) or thapsigargin (2 µM) increased it. Moreover, acetylcholine (100 µM) did not increase CBF in distal airway ciliary cells, although it increased CBF in tracheal ciliary cells. Terbutaline (10 µM), a selective ß2-adrenergic agonist, increased CBF in both tracheal and distal airway ciliary cells. These observations suggest that the Ca2+-mobilization mechanisms via purinergic or muscarinic receptors of the distal airway ciliary cell may be different from those of the tracheal ciliary cell. In conclusion, the CBF increase is differently regulated in the tracheal and distal airway epithelia of the rat.

(Received 21 September 2004; accepted after revision 4 March 2005; first published online 15 March 2005)
Corresponding author T. Nakahari: Department of Physiology, Osaka Medical College, Takatsuki, Osaka 569-8686, Japan. Email: takan{at}art.osaka-med.ac.jp




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