Demonstration of glibenclamide-sensitive K+ fluxes in rat liver mitochondria.
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.
Belyaeva
E A
EA
Nencki Institute of Experimental Biology, Warsaw, Poland.
Szewczyk
A
A
Mikołajek
B
B
Nałecz
M J
MJ
Wojtczak
L
L
D000818:Animals; D005905:Glyburide / Q000494:pharmacology*; D006146:Guanidines / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials; D008930:Mitochondria, Liver / Q000187:drug effects* / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D020110:Pinacidil; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar
D006146:Guanidines; D015221:Potassium Channels; C058754:N'-cyano-N-(3-pyridyl)-N''-(t-butyl)guanidine; D020110:Pinacidil; D011188:Potassium; D010100:Oxygen; D005905:Glyburide