Two-pore K + channels, NO and metabolic inhibition

Ischemic preconditioning is a potent endogenous mechanism protecting many organs from the devastating effects of prolonged ischemia. In the heart, NO is one mediator of this myoprotective response thought to involve activation of the K ATP channel. Ischemic preconditioning is known to be induced by...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2007-11, Vol.363 (1), p.194-196
Main Authors: Lu, Zhongju, Gao, Junyuan, Zuckerman, Joan, Mathias, Richard T., Gaudette, Glenn, Krukenkamp, Irvin, Cohen, Ira S.
Format: Article
Language:English
Subjects:
Animals
Cell Hypoxia
Cells, Cultured
Energy Metabolism - drug effects
Guinea Pigs
Ion channel
Ion Channel Gating - drug effects
Ion Channel Gating - physiology
Ischemic preconditioning
Membrane Potentials - drug effects
Membrane Potentials - physiology
Metabolic Clearance Rate - drug effects
Myocytes, Cardiac - drug effects
Myocytes, Cardiac - metabolism
Nitric Oxide - metabolism
Porosity
Potassium Channel Blockers - administration & dosage
Potassium Channels - drug effects
Potassium Channels - physiology
Sodium Cyanide - administration & dosage
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Summary:Ischemic preconditioning is a potent endogenous mechanism protecting many organs from the devastating effects of prolonged ischemia. In the heart, NO is one mediator of this myoprotective response thought to involve activation of the K ATP channel. Ischemic preconditioning is known to be induced by metabolic inhibition using sodium cyanide (NaCN) in single cardiomyocytes. In the present study, we show for the first time that the end effector channel activated by NaCN has been incorrectly identified. The channel activated is not K ATP but instead belongs to the relatively new family of two-pore domain potassium channels (K2P). Further when activated by metabolic ischemia, the amplitude of K2P current is directly modulated by activators and inhibitors of the NO pathway.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2007.08.131