Article date: June 1997
By: J. Tamaoki, E. Tagaya, K. Isono, M. Kondo, K. Konno, in Volume 121, Issue 4, pages 794-798
To elucidate whether K+ channels play a role in the action of epithelium‐dependent bronchodilatation, we studied responses in human bronchial strips in the presence of indomethacin and NG‐nitro‐L‐arginine methylester under isometric conditions, in vitro.
Mechanical removal of the epithelium increased the contractile responses to acetylcholine; the pD2 values increased from 5.0±0.2 to 5.9±0.3 (P<0.001). This potentiation was abolished by iberiotoxin but not by apamin or glibenclamide.
In cascade bioassay, application of the bathing medium from dispersed, bronchial epithelial cells to epithelium‐denuded bronchial strips decreased acetylcholine‐induced contraction by 44±6%. This effect was reduced to 10±3% (P<0.01) when the epithelial cells were pretreated with iberiotoxin, and to 4±1% (P<0.001) when the epithelial cells were incubated with Ca2+‐free medium containing [1,2‐bis (2) aminophenoxy] ethane N,N,N′,N′‐tetraacetic acid‐acetomethoxy ester.
In contrast, the bronchodilator effect of the medium bathing epithelial cells was not altered by the direct addition of iberiotoxin to epithelium‐denuded tissues.
These results suggest that the Ca2+‐activated K+ channel may play a role in the synthesis and/or release of smooth muscle relaxing factor, which is neither nitric oxide nor a cyclo‐oxygenase product, from airway epithelial cells.
To elucidate whether K+ channels play a role in the action of epithelium‐dependent bronchodilatation, we studied responses in human bronchial strips in the presence of indomethacin and NG‐nitro‐L‐arginine methylester under isometric conditions, in vitro.
Mechanical removal of the epithelium increased the contractile responses to acetylcholine; the pD2 values increased from 5.0±0.2 to 5.9±0.3 (P<0.001). This potentiation was abolished by iberiotoxin but not by apamin or glibenclamide.
In cascade bioassay, application of the bathing medium from dispersed, bronchial epithelial cells to epithelium‐denuded bronchial strips decreased acetylcholine‐induced contraction by 44±6%. This effect was reduced to 10±3% (P<0.01) when the epithelial cells were pretreated with iberiotoxin, and to 4±1% (P<0.001) when the epithelial cells were incubated with Ca2+‐free medium containing [1,2‐bis (2) aminophenoxy] ethane N,N,N′,N′‐tetraacetic acid‐acetomethoxy ester.
In contrast, the bronchodilator effect of the medium bathing epithelial cells was not altered by the direct addition of iberiotoxin to epithelium‐denuded tissues.
These results suggest that the Ca2+‐activated K+ channel may play a role in the synthesis and/or release of smooth muscle relaxing factor, which is neither nitric oxide nor a cyclo‐oxygenase product, from airway epithelial cells.
British Journal of Pharmacology (1997) 121, 794–798; doi:10.1038/sj.bjp.0701183
DOI: 10.1038/sj.bjp.0701183
View this article