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Am J Physiol Cell Physiol 280: C100-C109, 2001;
0363-6143/01 $5.00
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Vol. 280, Issue 1, C100-C109, January 2001

Role of calcium and calmodulin in ciliary stimulation induced by acetylcholine

Orna Zagoory, Alex Braiman, Larisa Gheber, and Zvi Priel

Department of Chemistry, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel

The goal of this work was to elucidate the molecular events underlying stimulation of ciliary beat frequency (CBF) induced by acetylcholine (ACh) in frog esophagus epithelium. ACh induces a profound increase in CBF and in intracellular Ca2+ concentration ([Ca2+]i) through M1 and M3 muscarinic receptors. The [Ca2+]i slowly decays to the basal level, while CBF stabilizes at an elevated level. These results suggest that ACh triggers Ca2+-correlated and -uncorrelated modes of ciliary stimulation. ACh response is abolished by the phospholipase C (PLC) inhibitor U-73122 and by depletion of intracellular Ca2+ stores but is unaffected by reduction of extracellular Ca2+ concentration and by blockers of Ca2+ influx. Therefore, ACh activates PLC and mobilizes Ca2+ solely from intracellular stores. The calmodulin inhibitors W-7 and calmidazolium attenuate the ACh-induced increase in [Ca2+]i but completely abolish the elevation in CBF. Therefore, elevation of [Ca2+]i is necessary for CBF enhancement but does not lead directly to it. The combined effect of Ca2+ elevation and of additional factors, presumably mobilized by Ca2+-calmodulin, results in a robust CBF enhancement.

cilia; mucociliary tissue; thapsigargin; cholinergic receptors; atropine


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