Induction of a glibenclamide-sensitive K-current by modification of a delayed rectifier channel in rat portal vein in insulinoma cells

In insulinoma cells (RINm5F), the glibenclamide-sensitive K-current (IK(ATP)) which developed spontaneously or after exposure to levcromakalim or to butanedione monoxime was always accompanied by a reduction in the delayed rectifier current (IK(V)). At potentials over which IK(V) was fully activated...

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Bibliographic Details
Published in:British journal of pharmacology Vol. 110; no. 4; p. 1280
Main Authors: Edwards, G, Weston, A H
Format: Journal Article
Language:English
Published: England 01.12.1993
Subjects:
Animals
Benzopyrans - pharmacology
Cromakalim
Glyburide - pharmacology
Insulinoma - metabolism
Neurotoxins - pharmacology
Phosphorylation
Portal Vein - drug effects
Portal Vein - metabolism
Potassium Channels - drug effects
Potassium Channels - physiology
Pyrroles - pharmacology
Rats
Scorpion Venoms
Tumor Cells, Cultured
ISSN:0007-1188
Online Access:Get more information
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Summary:In insulinoma cells (RINm5F), the glibenclamide-sensitive K-current (IK(ATP)) which developed spontaneously or after exposure to levcromakalim or to butanedione monoxime was always accompanied by a reduction in the delayed rectifier current (IK(V)). At potentials over which IK(V) was fully activated, the total outward current remained constant. In rat portal vein, the delayed rectifier channel inhibitor, margatoxin, reduced the combined induction of IK(ATP) and inhibition of IK(V) by levcromakalim. These data suggest that the ATP-sensitive K-channel, K(ATP), is a voltage-insensitive state of the delayed rectifier, KV.
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ISSN:0007-1188
DOI:10.1111/j.1476-5381.1993.tb13955.x