MitoK(ATP)-dependent changes in mitochondrial volume and in complex II activity during ischemic and pharmacological preconditioning of Langendorff-perfused rat heart.

Abstract	It has been proposed that activation of the mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) is part of signaling pathways triggering the cardioprotection afforded by ischemic preconditioning of the heart. This work was to analyze the mitochondrial function profile of Langendorff-perfused rat hearts during the different phases of various ischemia-reperfusion protocols. Specifically, skinned fibers of ischemic preconditioned hearts exhibit a decline in the succinate-supported respiration and complex II activity during ischemia, followed by a recovery during reperfusion. Meanwhile, the apparent affinity of respiration for ADP (which reflects the matrix volume expansion) is increased during preconditioning stimulus and, to a larger extent, during prolonged ischemia. This evolution pattern is mimicked by diazoxide and abolished by 5-hydroxydecanoate. It is concluded that opening the mitoK(ATP) channel mediates the preservation of mitochondrial structure-function via a mitochondrial matrix shrinkage and a reversible inactivation of complex II during prolonged ischemic insult.
Authors	Philippe Pasdois, Bertrand Beauvoit, Liliane Tariosse, Béatrice Vinassa, Simone Bonoron-Adèle, Pierre Dos Santos
Journal	Journal of bioenergetics and biomembranes (J Bioenerg Biomembr) Vol. 38 Issue 2 Pg. 101-12 (Apr 2006) ISSN: 0145-479X [Print] United States
PMID	17031549 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Antihypertensive Agents Decanoic Acids Hydroxy Acids Potassium Channels mitochondrial K(ATP) channel Adenosine Diphosphate 5-hydroxydecanoic acid Succinic Acid Electron Transport Complex II Diazoxide
Topics	Adenosine Diphosphate (metabolism) Animals Antihypertensive Agents (pharmacology) Cell Respiration (physiology) Decanoic Acids (pharmacology) Diazoxide (pharmacology) Electron Transport Complex II (physiology) Hydroxy Acids (pharmacology) In Vitro Techniques Ischemic Preconditioning, Myocardial Male Mitochondria, Heart (drug effects, physiology) Mitochondrial Size Myocardial Ischemia (metabolism) Myocardial Reperfusion Myofibrils (drug effects, physiology) Potassium Channels (metabolism) Rats Rats, Sprague-Dawley Succinic Acid (metabolism)

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