ArticleThe Journal of physiology1995
Activation of ATP-dependent K+ channels by metabolic poisoning in adult mouse skeletal muscle: role of intracellular Mg(2+) and pH.
Article in The Journal of physiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- KThe Journal of physiology · 2023Article
- A mechano- and heat-gated two-pore domain KProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Exercise and fatigue: integrating the role of KEuropean journal of applied physiology · 2023Review
- KATP channel deficiency in mouse FDB causes an impairment of energy metabolism during fatigue.American journal of physiology. Cell physiology · 2016Article
- K(ATP) channels process nucleotide signals in muscle thermogenic response.Critical reviews in biochemistry and molecular biology · 2010Article
- Adenosine triphosphate depletion by cyanide results in a Na(+)-dependent Mg(2+) extrusion from liver cells.Metabolism: clinical and experimental · 2010Article
- Muscle KATP channels: recent insights to energy sensing and myoprotection.Physiological reviews · 2010Review
- Regulation of ClC-1 and KATP channels in action potential-firing fast-twitch muscle fibers.The Journal of general physiology · 2009Article
- Sarcolemmal ion channels in dystrophin-deficient skeletal muscle fibres.Journal of muscle research and cell motility · 2006Review
- Role of adenosine A1 and A3 receptors in regulation of cardiomyocyte homeostasis after mitochondrial respiratory chain injury.American journal of physiology. Heart and circulatory physiology · 2005Article
- Allosteric modulation of the mouse Kir6.2 channel by intracellular H+ and ATP.The Journal of physiology · 2002Article
- Dual actions of the metabolic inhibitor, sodium azide on K(ATP) channel currents in the rat CRI-G1 insulinoma cell line.British journal of pharmacology · 1999Article
- Hypoxia activates ATP-dependent potassium channels in inspiratory neurones of neonatal mice.The Journal of physiology · 1998Article
- Similarity of ATP-dependent K+ channels in skeletal muscle fibres from normal and mutant mdx mice.The Journal of physiology · 1997Article
- Binding of [3H]-P1075, an opener of ATP-sensitive K+ channels, to rat glomerular preparations.Naunyn-Schmiedeberg's archives of pharmacology · 1996Article
- Intracellular Ca2+ changes and Ca2+-activated K+ channel activation induced by acetylcholine at the endplate of mouse skeletal muscle fibres.The Journal of physiology · 1996Article
- Cell-type specificity of preconditioning in an in vitro model.Basic research in cardiologyArticle
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effects of metabolic poisoning, intracellular Mg(2+) and pH on ATP-dependent K+ (K+ATP) channels were examined in adult mouse isolated skeletal muscle fibres using the patch clamp technique. 2. In cell-attached membrane patches, while openings of one kind of channel could only rarely be detected under control conditions, cell poisoning with fluorodinitrobenzene (FDNB), dinitrophenol (DNP) and cyanide (CN) induced a strong and partially reversible increase in channel activity. 3. Slope conductance and glibenclamide sensitivity of this outward current indicated that the channel activated during poisoning was the K+ATP channel. 4. Single channel current amplitude was reduced during poisoning, but remained unchanged when activation of the K+ATP channel was induced by cromakalim. 5. In inside-out membrane patches, in the absence of intracellular ATP, intracellular application of Mg2+ decreased channel activity and single channel current amplitude. Inhibition of K+ATP channels by ATP was also reduced. 6. In the absence of intracellular ATP, a decrease in intracellular pH induced a reduction in channel activity and single channel current amplitude. Inhibition of K+ATP channels by ATP was also reduced. 7. The reduction of single channel current amplitude during poisoning was attributed to an increase in intracellular Mg2+ concentration caused by a fall in intracellular ATP concentration. These results also show that metabolic poisoning causes direct activation of K+ATP channels in skeletal muscle, and that is activation is at least partially mediated through an increase in intracellular Mg(2+) concentration and a decrease in intracellular pH.
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