Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 363, Issue 1, Pages 194-196Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2007.08.131
Keywords
ischemic preconditioning; ion channel; NO
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Funding
- NHLBI NIH HHS [R01 HL070161, R01 HL070161-01A1, R01 HL067101-06A1, HL28958, R01 HL085221, R01 HL067101, R01 HL085221-01, HL67101, HL85221, P01 HL028958, P01 HL028958-210008] Funding Source: Medline
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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. (C) 2007 Elsevier Inc. All rights reserved.
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