Opening of Potassium Channels Protects Mitochondrial Function from Calcium Overload

Crestanello, Juan A.; Doliba, Nicolai M.; Babsky, Andriy M.; Doliba, Natalia M.; Niibori, Koki; Osbakken, Mary D.; Whitman, Glenn J.R.

doi:10.1006/jsre.2000.5979

Cited by 44 publications

(22 citation statements)

References 31 publications

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“…3, traces 8, 9). The results are in agreement with the data of other authors [9,11,13] and indicate that pinacidil, unlike Ca 2+ , has little effect on mito chondrial energetics.…”

supporting

confidence: 93%

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Effects of pinacidil and calcium on isolated rat heart mitochondria

Коротков

Emelyanova

Brailovskaya

et al. 2012

Dokl Biochem Biophys

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“…3, traces 8, 9). The results are in agreement with the data of other authors [9,11,13] and indicate that pinacidil, unlike Ca 2+ , has little effect on mito chondrial energetics.…”

supporting

confidence: 93%

“…Pinacidil was shown to activate respiration of iso lated mitochondria in states 2 and 4 [1,3,[9][10][11][12][13]. However, mitochondrial respiration in state 3 and the ATP synthesis rate are changed only slightly [9,13].…”

mentioning

confidence: 97%

Effects of pinacidil and calcium on isolated rat heart mitochondria

Коротков

Emelyanova

Brailovskaya

et al. 2012

Dokl Biochem Biophys

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“…It has been shown that K AT P channel openers such as pinacidil, cromakalim, and nicorandil modulate mitochondrial membrane potential, respiration, ATP generation, and mitochondrial Ca 2+ level [11,12]. The protective effect of K AT P channel activation could be mediated by mitochondrial swelling and it may improve mitochondrial ATP production [13], lowering Ca 2+ overloading of mitochondria [11,14], activation of protein kinase C by increased reactive oxygen species generation, which is known to be important during protection [15]. K AT P channels could act as sensors of cell energy metabolism [16].…”

Section: Introductionmentioning

confidence: 99%

Protective role of pinacidil against adrenaline-induced myocardium injury in guinea pig liver mitochondria

Tkachenko

Kurhalyuk²

2007

Open Life Sciences

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Abstract:We investigated the role of the ATP-sensitive potassium channel opener pinacidil and blocker glibenclamide on guinea pig liver mitochondrial function, and a possible significance of pinacidil in the pharmacological treatment during myocardium dystrophy. First, a series of experiments was performed to determine the effect of pinacidil and glibenclamide on mitochondrial oxygen consumption. We found that pinacidil increased the rate of mitochondrial respiration for FAD-generated substrate (succinate oxidation), but was most effective for α-ketoglutarate oxidation with enhancement of respiratory control ratio. Oxidation of FAD-generated substrate inhibited efficiency of phosphorylation for α-ketoglutarate oxidation in pinacidil-treated animals. Glibenclamide decreased the rate of respiration with the lowest value of efficiency of phosphorylation, especially for α-ketoglutarate oxidation. A second series of experiments was performed to determine the effects of pinacidil and glibenclamide on oxidative phosphorylation during adrenaline-induced myocardium dystrophy. The increase in respiratory control ratio and efficiency of phosphorylation for α-ketoglutarate oxidation was greater than for succinate oxidation in mitochondria of pinacidil-pretreated animals during myocardium dystrophy. Inhibitory analysis with malonate suggested that endogenous succinate increased oxidation of NADH-generated substrates in mitochondria. Pinacidil is mainly involved in the adrenaline-induced alterations of mitochondrial function due to elevation of phosphorylation efficiency for α-ketoglutarate oxidation and a decreased level of lipid peroxidation.

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“…IPC has been reported to protect the heart by reducing intracellular calcium and mitochondrial calcium accumulation. The underlying mechanism for this beneficial effect of IPC on calcium handling is unclear, and has been attributed to opening of the sarcolemmal K ATP channel (with action potential duration shortening) [81], opening of the MitoK ATP channel (with partial mitochondrial membrane depolarization and less mitochondrial calcium accumulation) [82][83][84][85][86][87][88][89][90], and reduced intracellular acidosis during myocardial ischemia (see previous section) [72].…”

Section: Ipc and Calciummentioning

confidence: 99%

Cardioprotection Techniques: Preconditioning, Postconditioning and Remote Con-ditioning (Basic Science)

Hausenloy¹

2013

CPD

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Ischemic heart disease (IHD) is the leading cause of death and disability worldwide. The major pathological consequences of IHD arise from the detrimental effects of acute ischemia-reperfusion injury (IRI) on the myocardium. Therefore, in order to improve clinical outcomes in patients with IHD, novel therapeutic strategies are required to protect the myocardium from acute IRI and preserve cardiac function (cardioprotection). In this regard, endogenous cardioprotective strategies such as ischemic preconditioning (IPC), ischemic postconditioning (IPost) and remote ischemic conditioning (RIC) may provide novel approaches for protecting the heart in clinical settings in which the patient experiences acute myocardial IRI. In this review article, we provide an overview of these endogenous cardioprotective strategies with respect to the pre-clinical experimental literature, exploring their major characteristics and underlying signaling mechanisms. The application of these therapeutic strategies in the clinical setting for potential patient benefit is reviewed in another article in this special issue.

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Opening of Potassium Channels Protects Mitochondrial Function from Calcium Overload

Cited by 44 publications

References 31 publications

Effects of pinacidil and calcium on isolated rat heart mitochondria

Effects of pinacidil and calcium on isolated rat heart mitochondria

Protective role of pinacidil against adrenaline-induced myocardium injury in guinea pig liver mitochondria

Cardioprotection Techniques: Preconditioning, Postconditioning and Remote Con-ditioning (Basic Science)

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