Abstract
The purpose of this study was to investigate the role of K+ channels in duodenal dismotility induced by ethanol in vitro. The amplitude of spontaneous contractions was reduced by ethanol in longitudinal and circular muscle, while frequency did not change. Charybdotoxin antagonized ethanol-induced inhibition of the amplitude of spontaneous contractions. Ethanol decreased ACh-induced contractions and this effect was cancelled out by charybdotoxin. Ca2+-activated K+ channels may be involved in duodenal dismotility induced by ethanol.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Acetylcholine / pharmacology
-
Animals
-
Central Nervous System Depressants / antagonists & inhibitors
-
Central Nervous System Depressants / pharmacology*
-
Charybdotoxin / pharmacology
-
Data Interpretation, Statistical
-
Duodenum / drug effects*
-
Duodenum / metabolism
-
Ethanol / antagonists & inhibitors
-
Ethanol / pharmacology*
-
Gastrointestinal Motility / drug effects*
-
In Vitro Techniques
-
Male
-
Muscle Contraction / drug effects
-
Muscle, Smooth / cytology
-
Muscle, Smooth / drug effects
-
Muscle, Smooth / metabolism
-
Peptides / pharmacology
-
Potassium Channel Blockers / pharmacology
-
Potassium Channels, Calcium-Activated / drug effects
-
Potassium Channels, Calcium-Activated / physiology*
-
Rabbits
-
Solutions
Substances
-
Central Nervous System Depressants
-
Peptides
-
Potassium Channel Blockers
-
Potassium Channels, Calcium-Activated
-
Solutions
-
Charybdotoxin
-
Ethanol
-
iberiotoxin
-
Acetylcholine