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
Summary
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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