Delayed pharmacological pre‐conditioning effect of mitochondrial ATP‐sensitive potassium channel opener on neurologic injury in a rabbit model of spinal cord ischemia

Kim, Kyoung Ok; Choe, Gyu-Ha; Chung, Soojie; Kim, C S

doi:10.1111/j.1399-6576.2007.01534.x

Cited by 5 publications

(1 citation statement)

References 30 publications

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“…Activation of mitochondrial K ATP channels initiates ischemic pre-conditioning and prevents the mitochondrial dysfunction associated with Ca 2+ overload during ischemic reperfusion in the heart [116][117][118] . In adult animals, application of mitochondrial K ATP openers, such as diazoxide or BMS-191095, reduces neuronal death (rats: [116,[119][120][121] ; mice: [122] ), whereas a selective mitochondrial K ATP channel blocker, 5-hydroxydecanoate, prevents preconditioning-induced neuronal protection in middle cerebral artery occlusion (MCAO) focal cerebral ischemia [123] .…”

Section: K Atp Channels and Their Neuroprotective Role In Cerebral Ismentioning

confidence: 99%

Neuroprotective role of ATP-sensitive potassium channels in cerebral ischemia

Sun

Feng

2012

Acta Pharmacol Sin

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ATP-sensitive potassium (K ATP ) channels are weak, inward rectifiers that couple metabolic status to cell membrane electrical activity, thus modulating many cellular functions. An increase in the ADP/ATP ratio opens K ATP channels, leading to membrane hyperpolarization. K ATP channels are ubiquitously expressed in neurons located in different regions of the brain, including the hippocampus and cortex. Brief hypoxia triggers membrane hyperpolarization in these central neurons. In vivo animal studies confirmed that knocking out the Kir6.2 subunit of the K ATP channels increases ischemic infarction, and overexpression of the Kir6.2 subunit reduces neuronal injury from ischemic insults. These findings provide the basis for a practical strategy whereby activation of endogenous K ATP channels reduces cellular damage resulting from cerebral ischemic stroke. K ATP channel modulators may prove to be clinically useful as part of a combination therapy for stroke management in the future.

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