Cited by 1,208Ion channel regulation and functionPancreatic function and diabetesIon Transport and Channel Regulation

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Intracellular ATP directly blocks K+ channels in pancreatic B-cells

Cook, Daniel L., Hales, Nicholas·1984·Nature

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Abstract

It is known that glucose-induced depolarization of pancreatic B-cells is due to reduced membrane K+-permeability and is coupled to an increase in the rate of glycolysis, but there has been no direct evidence linking specific metabolic processes or products to the closing of membrane K+ channels. During patch-clamp studies of proton inhibition of Ca2+-activated K+ channels [GK(Ca)] in B-cells, we identified a second K+-selective channel which is rapidly and reversibly inhibited by ATP applied to the cytoplasmic surface of the membrane. This channel is spontaneously active in excised patches and frequently coexists with GK(Ca) channels yet is insensitive to membrane potential and to intracellular free Ca2+ and pH. Blocking of the channel is ATP-specific and appears not to require metabolism of the ATP. This ATP-sensitive K+ channel [GK(ATP)] may be a link between metabolism and membrane K+-permeability in pancreatic B-cells.

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Background
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“…channels (KATP-channel) have been found to be distributed widely among various cells, such as cardiac cells (Noma, 1983), pancreaticb- ells (Cook & Hales, 1984; Findlay, Dunne & Petersen, 1985), skeletal muscle cells (Spruce, Standen & Stanfield, 1985), smooth muscle cells (Standen et al.,…”
Background
Glucagon induces Ca2+-dependent increase of reduced pyridine nucleotides in mouse pancreatic beta-cells.
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Cardiovascular Profile of E4080 and Its Analogue ER001533: Novel Potassium Channel Openers with Bradycardic Properties
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Effect of glibenclamide, a selective blocker of an ATP-K+ channel, on the anoxic response of hippocampal neurones
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“1985) cultured pancreatic B-cells (Cook and Hales 1984; Ashcroft et al. 1984; Findlay et al. 1985) and insulin secreting cell lines (Dunne et al.”
Background
Disopyramide and Its Metabolite Enhance Insulin Release from Clonal Pancreatic β-Cells by Blocking KATP Channels
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CHAPTER 15 – Inwardly-Rectifying K+ Channels in the Heart
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Metabolic Events that May Activate Erythropoietin Production in the Hypoxic Kidney
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Electrophysiological Measurements Show Marked Differences in the Properties of the Pancreatic β-Cell K-Channels from Albino Mice and a Strain of ob/ob (Obese) Mice
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The Amount of Releasable Insulin Depends on Continuous Oxidative Phosphorylation
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“3 , 4 7 A vast number of experimental observations lend support to this model, for example, the inhibition of insulin secretion by inhibitors of oxidative phosphorylation, 8 by K ATP channel openers 9 and by Ca 2 + channel blockers.”
Bayliss–Starling Prize Lecture: KATP channel pathophysiology – a whole‐body odyssey
Nichols, C. G. (2025) · The Journal of Physiology · doi:10.1113/jp287415 · Cited by 2
“Similar ATP-sensitive potassium (K ATP ) channels were soon identified in pancreatic β -cells (Cook & Hales, 1984), as well as in neurons (Ashcroft, 1988), skeletal muscle (Spruce et al., 1985), vascular (Standen et al., 1989) and lymphatic (von der Weid, 1998) smooth muscle myocytes.”
Sugar‐sensing swodkoreceptors and swodkocrine signaling
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Glucose-sensitivity of the afterhyperpolarization potential: Role of SK1 channel in insulin-secreting cells
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Hiperglicemia Induzida por Fluoxetina em Ratos Tratados com Glibenclamida
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Effects of Radical Scavengers, TA248 and TA276, on Stunned Myocardium in Dogs: Involvement of KATP Channels
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Hippocampal hypoglycaemia-activated K+ channels: single-channel analysis of glucose and voltage dependence
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“Since the first demonstrations in heart [15] and pancreatic fl-cells [3, 10], ATP-sensitive K + (KATP) channels have”
Background
Is sodium necessary for stimulus-secretion coupling in toad (caudiverbera caudiverbera) adrenal chromaffin cells?
Nassar‐Gentina, V., Aguilar, P., & Luxoro, M. (1992) · Comparative Biochemistry and Physiology Part A Physiology · doi:10.1016/0300-9629(92)90735-9 · Cited by 2
Molecular Mechanisms of Insulin Secretion and Insulin Action.
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ACETAZOLAMIDE SLOWS DOWN THE GLUCOSE-INDUCED MEMBRANE DEPOLARIZATION IN PANCREATIC B-CELLS: THE H+-SENSITIVE K+-PERMEABILITY IS RESPONSIBLE FOR THE DEPOLARIZATION
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Immunological techniques in diabetes research: 14 years on
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“w h i c h is d i r ec t ly c o n t r o l l e d b y A T P [45].”
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Contributions of Mitochondrial Dysfunction to β Cell Failure in Diabetes Mellitus
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Authors: Cook, D. L., & Hales, N.
Affiliations: United States Department of Veterans Affairs (US)
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 1984-09
Volume: 311
Issue: 5983
Pages: 271-273
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/311271a0
OpenAlex: W1985770721
Cited by: 1,208
References: 24
Citations by year: 2026: 11 · 2025: 16 · 2024: 12 · 2023: 22 · 2022: 14 · 2021: 21 · 2020: 12 · 2019: 19 · 2018: 13 · 2017: 9 · 2016: 15 · 2015: 21 · 2014: 34 · 2013: 14 · 2012: 29
FWCI: 13.20
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords: ATP-sensitive potassium channels, pancreatic beta cells, intracellular ATP, potassium channel inhibition, glycolysis, proton inhibition, calcium-activated potassium channels
MeSH terms: Adenosine Triphosphate, Animals, Cell Membrane Permeability, Cells, Cultured, Cytoplasm, Electric Conductivity, Ion Channels, Islets of Langerhans, Potassium, Rats

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Intracellular ATP directly blocks K+ channels in pancreatic B-cells

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