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Effects of K + channel inhibitors on the basal tone and KCl- or methacholine-induced contraction of mouse trachea

The present study examined the effects of K + channel inhibitors on the basal tone and on KCl- or methacholine-induced contraction of the mouse-isolated trachea. Glibenclamide and iberiotoxin, procaine, quinine and tetraethylammonium did not induce any contraction of the indomethacin-treated mouse t...

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Bibliographic Details
Published in:European journal of pharmacology 1998-04, Vol.346 (2), p.255-260
Main Authors: Li, Liang, Paakkari, Ilari, Vapaatalo, Heikki
Format: Article
Language:English
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Summary:The present study examined the effects of K + channel inhibitors on the basal tone and on KCl- or methacholine-induced contraction of the mouse-isolated trachea. Glibenclamide and iberiotoxin, procaine, quinine and tetraethylammonium did not induce any contraction of the indomethacin-treated mouse trachea. 4-Aminopyridine induced concentration-dependent contraction. This action of 4-aminopyridine was abolished by atropine and reduced by tetrodotoxin and nifedipine. Glibenclamide failed to modify KCl- or methacholine-induced contraction. Iberiotoxin and 4-aminopyridine potentiated KCl- and methacholine-induced contractions. Nifedipine, procaine, quinine and tetraethylammonium inhibited KCl- and methacholine-induced contractions. These data suggest that the closure of large Ca 2+-dependent K + channels can potentiate KCl- and methacholine-induced contraction. The effects of 4-aminopyridine on the mouse trachea reflect chiefly activation of muscarinic receptors. Procaine, quinine and tetraethylammonium inhibit depolarization-induced and receptor-mediated contractions of the mouse-isolated trachea.
ISSN:0014-2999
1879-0712
DOI:10.1016/S0014-2999(98)00074-0