Abstract

ATP-sensitive potassium transport in rat brain mitochondria is highly sensitive to mK(ATP) channels openers: a light scattering study

Highlights

  • Mitochondrial ATP-sensitive K+ transport driven by ATP-sensitive potassium channels afford cytoprotection in different cell types under several pathophysio­logical and metabolic stress conditions

  • As it was shown in multiple studies, neuro- and cardioprotection conferred by mK channels openers was largely based on bioenergetic effects of ATPsensitive K+ transport, which under pathophysiological conditions improved mitochondrial functions, reduced mitochondrial calcium loading and prevented the damage of mitochondrial Ca2+ overload, such as the opening of permeability transition pore

  • In this work we used light scattering to study the effects of diazoxide and pinacidil on the potassium uptake in native isolated mitochondria, in the absence of Mg2+ and ATP

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Summary

Introduction

Mitochondrial ATP-sensitive K+ transport driven by ATP-sensitive potassium channels (mKATP channels) afford cytoprotection in different cell types under several pathophysio­logical and metabolic stress conditions [1, 2]. Under ischemic and hypoxic conditions pharmacological mKATP channels openers (KCOs) used for mKATP channel activation effectively prevented the development of apoptosis and necrosis in the neurons [4,5,6]. Sis, Ca2+ transport and ROS production [1, 2, 4] As it was shown in multiple studies, neuro- and cardioprotection conferred by mK channels openers. The modulation of mitochondrial ROS production by ATP-sensitive K+ transport and triggering of cytoprotective signaling in several studies suppressed the development of apoptosis and cell death in neurons and other cell types [2, 4, 8]. The aim of this work was to study the effect of diazoxide and pinacidil on the ATP-sensitive K+ transport in brain mitochondria in the absence of MgATP

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