Demonstration of glibenclamide-sensitive K+ fluxes in rat liver mitochondria.

Abstract

Influx of K+ into rat liver mitochondria driven by the transmembrane potential was investigated. Under non-energized conditions (non-respiring mitochondria suspended in isotonic KSCN) K+ influx (manifested by mitochondrial swelling) was enhanced by pinacidil and its derivative P1060, known as K+ channel openers in the plasma membrane; this stimulation being inhibited by potassium channel blocker glibenclamide. Under energized conditions (respiring mitochondria) the rate of K+ uptake (measured with K(+)-sensitive electrode) was increased by P1060 and slowed down by glibenclamide. These results indicate functioning of a specific potassium channel in intact liver mitochondria.