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Hypo-osmotic potentiation of acetylcholine-stimulated ciliary beat frequency through ATP release in rat tracheal ciliary cells.

Authors
  • Kawakami, Manpei1
  • Nagira, Tomoyoshi
  • Hayashi, Tetsuya
  • Shimamoto, Chikao
  • Kubota, Takahiro
  • Mori, Hiroshi
  • Yoshida, Hideyo
  • Nakahari, Takashi
  • 1 Department of Thoracic and Cardiovascular Surgery, Osaka Medical College, Takatsuki 569-8686, Japan.
Type
Published Article
Journal
Experimental physiology
Publication Date
November 2004
Volume
89
Issue
6
Pages
739–751
Identifiers
PMID: 15364881
Source
Medline
License
Unknown

Abstract

The ciliary beat frequency (CBF) of rat tracheal ciliary cells in a slice preparation was measured using video-enhanced contrast (VEC) microscopy. Acetylcholine (ACh) increased CBF mediated via intracellular Ca2+ concentration ([Ca2+]i) in a dose-dependent manner. An adequate hypo-osmotic stress (-40 mosM) potentiated ACh-stimulated CBF increase in tracheal ciliary cells and shifted the ACh dose-response curve to the left (lower concentration side). This potentiation was independent of hypo-osmotic stresses applied ranging from -20 mosM to -90 mosM. A hypo-osmotic stress induces ATP release in many cell types. The present study demonstrated that suramin (an inhibitor of purinergic receptors) and apyrase (an ATPase/ADPase) eliminate the hypo-osmotic potentiation of ACh-stimulated CBF increase and that ATP increased [Ca2+]i and CBF, as well as potentiating ACh-stimulated rises in [Ca2+]i and CBF increase. Moreover, the apical surface of tracheal ciliary cells were stained immunopositive for the P2X4 purinergic receptor. A hypo-osmotic stress (-40 mosM) transiently increased [Ca2+]i and potentiated the ACh-stimulated [Ca2+]i increase. The hypo-osmotic potentiation of ACh-stimulated CBF increase was not detected under Ca2+-free conditions. These observations suggest that a hypo-osmotic stress stimulates ATP release from the trachea. The released ATP may induce further increases in [Ca2+]i and CBF in ACh-stimulated tracheal ciliary cells, which may be mediated by purinergic receptors, such as P2X4.

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