Muscarinic signaling in ciliated tracheal epithelial cells: Dual effects on Ca2+ and ciliary beating

Matthias Salathe, Eric J. Lipson, Pedro I. Ivonnet, Richard J. Bookman

Research output: Contribution to journalArticlepeer-review

55 Scopus citations


To examine cholinergic signal transduction pathways that modulate ciliary beat frequency (CBF), cultured ovine tracheal epithelial cells were imaged using a combination of phase-contrast (CBF) and fluorescence (Ca2+) microscopy techniques. In single cells, acetylcholine (ACh) transiently increased CBF and intracellular Ca2+ concentration ([Ca2+](i)), mainly by Ca2+ release from internal stores, with a small delayed contribution from Ca2+ influx. Nicotinic agonists did not alter CBF or [Ca2+](i), whereas atropine blocked the ACh-stimulated transients, consistent with the involvement of muscarinic receptors. 4-Diphenylacetoxy-N-methylpiperidine methiodide was ~100 times more potent than pirenzepine in inhibiting the ACh-induced [Ca2+](i) peaks, suggesting that the receptor is a pharmacologically defined (M3) subtype. Interestingly, after depletion of intracellular Ca2+ stores by thapsigargin, ACh caused a rapid transient decrease in both CBF and [Ca2+](i), again with an antagonist profile of M3 receptors. We conclude that activation of M3 muscarinic receptors initiates specific signaling pathways that act simultaneously to increase and decrease [Ca2+](i) and CBF.

Original languageEnglish (US)
Pages (from-to)L301-L310
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number2 16-2
StatePublished - Feb 1997
Externally publishedYes


  • cholinergic stimulation
  • ciliary beat frequency
  • G proteins
  • manganese quenching
  • muscarinic receptors
  • phospholipase C

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Cell Biology
  • Physiology
  • Physiology (medical)


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