Anoxia and Glucose-Sensitive 86Rb Outflow from Rat Portal Vein

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Abstract
Exposure of rat portal veins to an N2-gassed buffer markedly increased 86Rb outflow. Moreover, glucose caused a pronounced reduction in 86Rb outflow from portal veins perfused with an N2-gassed buffer. Pinacidil, cromakalim and diazoxide provoked a sustained increase in 86Rb outflow. The stimulatory effect of pinacidil was not impaired in the absence of extracellular Ca2+ but was completely abolished by glibenclamide. These observations are compatible with the involvement of a metabolic process in the control of the K+ permeability, namely with the existence in rat portal veins of ATP-sensitive K+ channels.

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