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Role of the mitochondrial ATP-sensitive Kplus channels in cardioprotection

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Ardehali H.

Acta Biochimica Polonica

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2004

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tom 51

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nr 2

The mitochondrial ATP-sensitive K+ (mitoKATP) channel was discovered more than a decade ago. Since then, several pharmacological studies have identified agents that target this channel some of which selectively target mitoKATP. These and other studies have also suggested that mitoKATP plays a key role in the process of ischemic preconditioning (IPC) and prevention of apoptosis. The mechanism by which mitoKATP exerts its protective effects is unclear, however, changes in mitochondrial Ca2+ uptake and levels of reactive oxygen species, and mitochondrial matrix swelling are believed to be involved. Despite major advances, several important issues regarding mitoKATP remain unanswered. These questions include, but are not limited to: the molecular structure of mitoKATP, the downstream and upstream mechanisms that leads to IPC and cell death, and the pharmacological profile of the channel. This review attempts to provide an up-to-date overview of the role of mitoKATP in cardioprotection.

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Endothelial protection from reperfusion injury by ischemic preconditioning and diazoxide involves a SOD-like anti-O2 mechanism

100%

Maczewski M., Duda M., Pawlak W., Beresewicz A.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 3

Cardiac ischemia/reperfusion leads to coronary endothelial dysfunction, mediated by superoxide anion (O2-), but not hydroxyl radical (.OH). Ischemic preconditioning and mitochondrial ATP-dependent potassium channel opener (diazoxide) protect endothelium in the mechanism involving attenuation of O2- burst at reperfusion. We hypothesize that the endothelial protection involves upregulation of myocardial anty-O2- defense. Langendorff-perfused guinea-pig hearts were subjected to global ischemia/reperfusion (IR) or were preconditioned prior to IR with three cycles of ischemia/reperfusion (IPC) or infusion/washout of 0.5 µM diazoxide. Coronary flow responses to acetylcholine were measures of endothelium-dependent vascular function. Myocardial outflow of O2- and of .OH during reperfusion and myocardial activities of superoxide dismutase (SOD) and catalase were measured. IR impaired acetylcholine response and augmented cardiac O2- and .OH outflow. IPC, diazoxide, and SOD (150 IU/ml) attenuated O2- outflow, increased .OH outflow and protected endothelium. There were no differences in Cu/Zn-SOD, Mn-SOD and catalase activities between sham-perfused and IR hearts and only catalase activity was increased in the IPC hearts. We speculate that: (i) IPC and diazoxide endothelial protection involves activation of some SOD-like anti-O2- mechanism resulting in attenuation of O2- burst and increase in .OH burst, (ii) improved SOD activity might have not been detected because it was confined to a small, although functionally important, enzyme fraction, like that bound to the endothelial glycocalyx.

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Influence of diazoxide on the function of mitochondria in guinea pig liver under myocardium dystrophy

84%

Kurhalyuk N., Tkachenko G.

Bulletin of the Veterinary Institute in Puławy

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2006

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tom 50

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nr 1

Ograniczanie wyników

1 Acta Biochimica Polonica

1 Bulletin of the Veterinary Institute in Puławy

1 Journal of Physiology and Pharmacology

1 Ardehali H.

1 Beresewicz A.

1 Duda M.

1 Kurhalyuk N.

1 Maczewski M.

1 Pawlak W.

1 Tkachenko G.

1 2006

2 2004

Role of the mitochondrial ATP-sensitive Kplus channels in cardioprotection

Endothelial protection from reperfusion injury by ischemic preconditioning and diazoxide involves a SOD-like anti-O2 mechanism

Influence of diazoxide on the function of mitochondria in guinea pig liver under myocardium dystrophy