Evidence map›Paper›PMID 11682455›Full record

ArticleBritish journal of pharmacology2001

Inhibition of acetylcholine-activated K(+) currents by U73122 is mediated by the inhibition of PIP(2)-channel interaction.

H Cho, J B Youm, S Y Ryu, Y E Earm, W K Ho

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In one paragraph

Article in British journal of pharmacology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Neuronal G protein-gated KAmerican journal of physiology. Cell physiology · 2022
    Review
  3. Review
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  5. Endoplasmic reticulum (ER) CaThe Journal of biological chemistry · 2017
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Channelopathies linked to plasma membrane phosphoinositides.Pflugers Archiv : European journal of physiology · 2010
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

H ChoNational Research Laboratory for Cellular Signalling, Seoul National University College of Medicine, 28 Yonkeun-Dong, Chongno-Ku, Seoul, 110-799, Korea.
J B Youm
S Y Ryu
Y E Earm
W K Ho
Seoul National University · KRCheju Halla University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. We have investigated the effect of U73122, a specific inhibitor of phospholipase C (PLC), on acetylcholine-activated K(+) currents (I(KACh)) in mouse atrial myocytes. 2. In perforated patch clamp mode, I(KACh) was activated by 10 microM acetylcholine. When atrial myocytes were pretreated with U73122 or U73343, I(KACh) was inhibited dose-dependently (half-maximal inhibition at 0.12+/-0.0085 and 0.16+/-0.0176 microM, respectively). The current-voltage relationships for I(KACh) in the absence and in the presence of U73122 showed that the inhibition occurred uniformly from -120 to +40 mV, indicating a voltage-independent inhibition. 3. When U73122 was applied after I(KACh) reached steady-state, a gradual decrease in I(KACh) was observed. The time course of the current decrease was well fitted to a single exponential, and the rate constant was proportional to the concentration of U73122. 4. When K(ACh) channels were directly activated by adding 1 mM GTP gamma S to the bath solution in inside-out patches, U73122 (1 microM) decreased the open probability significantly without change in mean open time. When K(ACh) channels were activated independently of G-protein activation by 20 mM Na(+), open probability was also inhibited by U73122. 5. Voltage-activated K(+) currents and inward rectifying K(+) currents were not affected by U73122. 6. These findings show that inhibition by U73122 and U73343 of K(ACh) channels occurs at a level downstream of the action of G beta gamma or Na(+) on channel activation. The interference with phosphatidylinositol 4,5-bisphosphate (PIP(2))-channel interaction can be suggested as a most plausible mechanism.

Indexed as

AcetylcholineAdenosine TriphosphateAnimalsAtrial FunctionDose-Response Relationship, DrugEstrenesGuanosine 5'-O-(3-Thiotriphosphate)Heart AtriaMembrane PotentialsMicePatch-Clamp TechniquesPhosphatidylinositol 4,5-DiphosphatePhosphodiesterase InhibitorsPotassium ChannelsPotassium Channels, Inwardly RectifyingProtein Binding1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dioneAcetylcholineAdenosine TriphosphateEstrenesGuanosine 5'-O-(3-Thiotriphosphate)Phosphatidylinositol 4,5-DiphosphatePhosphodiesterase InhibitorsPotassium ChannelsPotassium Channels, Inwardly RectifyingPyrrolidinonesSodium

Identifiers

PMID11682455
PMCPMC1573039
OpenAlexW2153604766

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.