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Cited by 96Ion channel regulation and functionPancreatic function and diabetesIon Transport and Channel Regulation

Block of ATP‐regulated and Ca2(+)‐activated K+ channels in mouse pancreatic beta‐cells by external tetraethylammonium and quinine.

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Bokvist, K, Rorsman, P, Smith, P A·1990·The Journal of Physiology
DOI 10.1113/jphysiol.1990.sp018025PMC PMC1189760
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Abstract

1. The whole‐cell and outside‐out patch configurations of the patch‐clamp technique were used to investigate the effects of extracellular tetraethylammonium ions (TEA+) and quinine on both Ca2(+)‐activated and ATP‐regulated K+ channels in mouse pancreatic beta‐cells. 2. The Ca2(+)‐activated K+ channel has a single‐channel K+ permeability of 4.7 x 10(‐13) cm3 s‐1 when recorded with physiological ionic gradients. This value decreased to 2.9 x 10(‐13) cm3 s‐1 after addition of 0.3 mM‐TEA+. 3. Two exponentials with time constants of 0.2 and 4.7 ms were required to describe the distribution of the channel openings suggesting that the Ca2(+)‐activated K+ channel has at least two open states. The fast and slow components comprised 16 and 84% of the total number of openings respectively. 4. TEA+ caused a concentration‐dependent decrease in the single‐channel amplitude and open probability of the Ca2(+)‐activated K+ channel. A Kd for the reduction in the mean current of 0.14 mM was observed. The stoichiometry was approximately 1:1. 5. Quinine blocked the Ca2(+)‐activated K+ channel in a concentration‐dependent manner. Half‐maximal block was observed at 0.10 mM and binding was 1:1. Inhibition by 20 microM‐quinine was not associated with a decrease in channel amplitude but markedly reduced the lifetime of the channel openings. Two exponentials, with time constants of 0.5 and 1.3 ms, were required to describe the channel openings. The rapid component contained 55% of the events. 6. TEA+ reduced the single‐channel amplitude of the ATP‐regulated K+ channel in a concentration‐dependent manner. Kd for the block was 22 mM and the binding approximately 1:1. The block was not associated with changes in the open probability or channel kinetics. Two exponentials were required to describe the distribution of the open times. The time constants for the fast and slow components were approximately 2 and approximately 20 ms respectively. The rapid component accounted for approximately 35% of the events. 7. Quinine (10‐20 microM) almost abolished activity of the ATP‐regulated K+ channels. Inhibition was characterized by slow onset and reversibility but not associated with a change in the appearance of the single‐channel events. Quinine‐induced block could not be reversed by diazoxide. 8. We conclude that TEA+ produces rapid block of both Ca2(+)‐activated and ATP‐regulated K+ channels.(ABSTRACT TRUNCATED AT 400 WORDS)

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  • BK channels are blocked by TEA with an IC50 of 100 μM, which is 15- and 200-fold lower than the corresponding values for the delayed rectifier and KATP channel, respectively.

    “BK channels are blocked by the broad-spectrum K+ channel blocker TEA with an IC50 of 100µM, which is 15- and 200-fold lower than the corresponding values for the delayed rectifier and KATP channel, respectively (75, 76).”

    From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [75]

    The indexed abstract (items 4 and 6; page not supplied) reports TEA block of Ca²⁺-activated K⁺ channels with a Kd of 0.14 mM (140 μM) and ATP-regulated K⁺ channels with a Kd of 22 mM. These support substantially greater sensitivity of the Ca²⁺-activated channel, but not the stated 100 μM value or an exact 200-fold difference (the reported values give about 157-fold). The copy does not give a delayed-rectifier TEA value from which to verify the 15-fold comparison. (LLM, conf=0.88)

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Cites

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Research works printed but not linked: 29

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Cited by

Sorted by citations

Authors
Bokvist, K., Rorsman, P., & Smith, P. A.
Affiliations
University of Gothenburg (SE)
ORCID
Venue
The Journal of Physiology
Publisher
Wiley
Published
1990-04
Volume
423
Issue
1
Pages
327-342
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
DOI
10.1113/jphysiol.1990.sp018025
PMC
PMC1189760
OpenAlex
W2081913797
Cited by
96
References
1
Citations by year
2026: 1 · 2025: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 1 · 2015: 2 · 2014: 3 · 2013: 2
FWCI
4.00
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • The Journal of Physiology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
ATP-sensitive potassium channels, calcium-activated potassium channels, tetraethylammonium, quinine, channel block, pancreatic beta cells, open probability, channel kinetics, channel stoichiometry, channel selectivity, ATP-gated ion channels
MeSH terms
Adenosine Triphosphate, Animals, Calcium, Electrophysiology, Islets of Langerhans, Kinetics, Quinine, Tetraethylammonium Compounds, Potassium Channels, Tetraethylammonium, Mice, In Vitro Techniques

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