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Induction of a glibenclamide‐sensitive K‐current by modification of a delayed rectifier channel in rat portal vein and insulinoma cells
Author(s) -
Edwards G.,
Weston A.H.
Publication year - 1993
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1993.tb13955.x
Subject(s) - glibenclamide , potassium channel , chemistry , endocrinology , medicine , patch clamp , inward rectifier potassium ion channel , insulinoma , biophysics , electrophysiology , biology , biochemistry , ion channel , pancreas , receptor , diabetes mellitus
In insulinoma cells (RINm5F), the glibenclamide‐sensitive K‐current ( I K(ATP) ) which developed spontaneously or after exposure to levcromakalim or to butanedione monoxime was always accompanied by a reduction in the delayed rectifier current ( I K(V) ). At potentials over which I K(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 I K(ATP) and inhibition of I K(V) by levcromakalim. These data suggest that the ATP‐sensitive K‐channel, K (ATP) , is a voltage‐insensitive state of the delayed rectifier, K V .