| Autor: |
Zagoory O; Department of Chemistry, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel., Braiman A, Gheber L, Priel Z |
| Jazyk: |
angličtina |
| Zdroj: |
American journal of physiology. Cell physiology [Am J Physiol Cell Physiol] 2001 Jan; Vol. 280 (1), pp. C100-9. |
| DOI: |
10.1152/ajpcell.2001.280.1.C100 |
| Abstrakt: |
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 Ca(2+) concentration ([Ca(2+)](i)) through M(1) and M(3) muscarinic receptors. The [Ca(2+)](i) slowly decays to the basal level, while CBF stabilizes at an elevated level. These results suggest that ACh triggers Ca(2+)-correlated and -uncorrelated modes of ciliary stimulation. ACh response is abolished by the phospholipase C (PLC) inhibitor U-73122 and by depletion of intracellular Ca(2+) stores but is unaffected by reduction of extracellular Ca(2+) concentration and by blockers of Ca(2+) influx. Therefore, ACh activates PLC and mobilizes Ca(2+) solely from intracellular stores. The calmodulin inhibitors W-7 and calmidazolium attenuate the ACh-induced increase in [Ca(2+)](i) but completely abolish the elevation in CBF. Therefore, elevation of [Ca(2+)](i) is necessary for CBF enhancement but does not lead directly to it. The combined effect of Ca(2+) elevation and of additional factors, presumably mobilized by Ca(2+)-calmodulin, results in a robust CBF enhancement. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
|
