Mitochondrial Atp Sensitive K Channels
Mostrando 1-12 de 13 artigos, teses e dissertações.
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1. Role of mitochondrial ATP-sensitive potassium channel-mediated PKC-ε in delayed protection against myocardial ischemia/reperfusion injury in isolated hearts of sevoflurane-preconditioned rats
This study aimed to determine the role of mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channels and protein kinase C (PKC)-ε in the delayed protective effects of sevoflurane preconditioning using Langendorff isolated heart perfusion models. Fifty-four isolated perfused rat hearts were randomly divided into 6 groups (n=9)
Braz J Med Biol Res. Publicado em: 27/03/2015
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2. Effect of a high fat diet on mitochondria: bioenergetics, K+ transport and redox state / Efeito de dietas hiperlipídicas sobre mitocôndrias de fígado de camundongos: bioenergética, transporte de K+ e estudo redox
Obesity is associated with multiple dysfunctions including dyslipidemia, insulin resistance and diabetes. These malfunctions are associated with modifications in mitochondrial physiology. Furthermore, mitochondria are the most important site of energy metabolism and reactive oxygen species production. Alberici et al. (2006) demonstrated that hypertriglycerid
Publicado em: 2009
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3. Efeitos redox e protetores do pré-condicionamento isquêmico e da abertura do canal mitocondrial de potássio sensível a ATP contra morte celular por isquemia e reperfusão cardíaca / Redox and Protective Effects of Ischemic Preconditioning and Mitochondrial ATP-Sensitive K+ Channels Against Cardiac Cell Death Promoted by Ischemia and Reperfusion
Eventos isquêmicos seguidos por reperfusão levam ao dano celular e mitocondrial devido à abertura do poro de transição de permeabilidade mitocondrial (TPM). Todavia, o pré-condicionamento evita o dano celular por isquemia e reperfusão. Esse efeito protetor é semelhante ao obtido pela abertura do canal mitocondrial de potássio sensível a ATP (mitoKA
Publicado em: 2007
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4. Mitochondrial K+ transport and cardiac protection during ischemia/reperfusion
Mitochondrial ion transport, oxidative phosphorylation, redox balance, and physical integrity are key factors in tissue survival following potentially damaging conditions such as ischemia/reperfusion. Recent research has demonstrated that pharmacologically activated inner mitochondrial membrane ATP-sensitive K+ channels (mitoK ATP) are strongly cardioprotect
Brazilian Journal of Medical and Biological Research. Publicado em: 2005-03
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5. Multiprotein complex containing succinate dehydrogenase confers mitochondrial ATP-sensitive K+ channel activity
The mitochondrial ATP-sensitive K+ (mitoKATP) channel plays a central role in protection of cardiac and neuronal cells against ischemia and apoptosis, but its molecular structure is unknown. Succinate dehydrogenase (SDH) is inhibited by mitoKATP activators, fueling the contrary view that SDH, rather than mitoKATP, is the target of cardioprotective drugs. Her
National Academy of Sciences.
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6. Adenylate kinase phosphotransfer communicates cellular energetic signals to ATP-sensitive potassium channels
Transduction of energetic signals into membrane electrical events governs vital cellular functions, ranging from hormone secretion and cytoprotection to appetite control and hair growth. Central to the regulation of such diverse cellular processes are the metabolism sensing ATP-sensitive K+ (KATP) channels. However, the mechanism that communicates metabolic
The National Academy of Sciences.
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7. Identification and properties of an ATP-sensitive K+ current in rabbit sino-atrial node pacemaker cells.
1. Single myocytes were isolated from rabbit sino-atrial (SA) node by enzymatic dissociation. Spontaneous pacemaker activity, whole-cell and single-channel currents were recorded under conditions known to modulate ATP-sensitive K+ (KATP) channels. 2. The KATP channel openers, cromakalim and pinacidil, slowed or abolished the pacemaker activity, and caused hy
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8. Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion
Heart tissue is remarkably sensitive to oxygen deprivation. Although heart cells, like those of most tissues, rapidly adapt to anoxic conditions, relatively short periods of ischaemia and subsequent reperfusion lead to extensive tissue death during cardiac infarction. Heart tissue is not readily regenerated, and permanent heart damage is the result. Although
Portland Press Ltd..
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9. Mitochondrial Dysfunction Contributes to Impaired Insulin Secretion in INS-1 Cells with Dominant-negative Mutations of HNF-1α and in HNF-1α-deficient Islets*
Maturity Onset Diabetes of the Young-type 3 (MODY-3) has been linked to mutations in the transcription factor hepatic nuclear factor (HNF)-1α, resulting in deficiency in glucose-stimulated insulin secretion. In INS-1 cells overexpressing doxycycline-inducible HNF-1α dominant-negative (DN-) gene mutations, and islets from Hnf-1α knock-out mice, insulin sec
American Society for Biochemistry and Molecular Biology.
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10. Activation of ATP-sensitive K+ (KATP) channels by H2O2 underlies glutamate-dependent inhibition of striatal dopamine release
In many cells, ATP-sensitive K+ channels (KATP channels) couple metabolic state to excitability. In pancreatic beta cells, for example, this coupling regulates insulin release. Although KATP channels are abundantly expressed in the brain, their physiological role and the factors that regulate them are poorly understood. One potential regulator is H2O2. We re
National Academy of Sciences.
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11. Protection of cardiac mitochondria by diazoxide and protein kinase C: Implications for ischemic preconditioning
Mitochondrial ATP-sensitive K (mitoKATP) channels play a central role in protecting the heart from injury in ischemic preconditioning. In isolated mitochondria exposed to elevated extramitochondrial Ca, Pi, and anoxia to simulate ischemic conditions, the selective mitoKATP channel agonist diazoxide (25–50 μM) potently reduced mitochondrial injury by preve
The National Academy of Sciences.
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12. Role of sarcolemmal KATP channels in cardioprotection against ischemia/reperfusion injury in mice
Recently it has been postulated that mitochondrial ATP-sensitive K+ (mitoKATP) channels rather than sarcolemmal KATP (sarcKATP) channels are important as end effectors and/or triggers of ischemic preconditioning (IPC). To define the pathophysiological significance of sarcKATP channels, we conducted functional experiments using Kir6.2-deficient (KO) mice. Met
American Society for Clinical Investigation.