Induction of a glibenclamide‐sensitive K‐current by modification of a delayed rectifier channel in rat portal vein and insulinoma cells
G Edwards, AH Weston - British journal of pharmacology, 1993 - Wiley Online Library
G Edwards, AH Weston
British journal of pharmacology, 1993•Wiley Online LibraryIn 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 …
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 …
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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