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

Abstract

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.