Evidence map›Paper›PMID 11744757›Full record

ArticleThe Journal of physiology2001

Activation of ATP-sensitive K(+) channels by epoxyeicosatrienoic acids in rat cardiac ventricular myocytes.

T Lu, T Hoshi, N L Weintraub, A A Spector, H C Lee

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 81 citations in OpenAlex.

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  12. Activity, inhibition, and induction of cytochrome P450 2J2 in adult human primary cardiomyocytes.Drug metabolism and disposition: the biological fate of chemicals · 2013
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  19. Article
  20. Eicosanoid signalling pathways in the heart.Cardiovascular research · 2009
    Review
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.

T LuDepartment of Internal Medicine, University of Iowa College of Medicine, Iowa City, IA 52242, USA.
T Hoshi
N L Weintraub
A A Spector
H C Lee
University of Iowa · USUnited States Department of Veterans Affairs · US

Funding

Vascular Protection During HypertensionP01HL062984 · NHLBI · UNIVERSITY OF IOWA · PI SIGMUND, CURT DANIEL · 2000 to 2015
$22.2M
REGULATION OF TG RICH LIPOPROTEIN SECRETION BY OXIDIZED LIPIDSP01HL049264 · NHLBI · UNIVERSITY OF IOWA · PI SPECTOR, ARTHUR A. · 1992 to 2001
$2.6M
EFFECTS OF EPOXYEICOSATRIENOIC ACIDS ON KATP CHANNELR01HL063754 · NHLBI · UNIVERSITY OF IOWA · PI LEE, HON-CHI · 2000 to 2003
$1.2M
REGULATION OF ION CHANNELS BY APOPTOSIS TRIGGER PROTEINSR01HL061645 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI HOSHI, TOSHINORI · 1999 to 2002
$613k
NHLBI NIH HHS HL-49264NHLBI NIH HHS HL-61645NHLBI NIH HHS HL-62984NHLBI NIH HHS HL-63754NHLBI NIH HHS P01 HL062984NHLBI NIH HHS R01 HL063754
6 · The paper itself

Abstract

1. We examined the effects of epoxyeicosatrienoic acids (EETs), which are cytochrome P450 metabolites of arachidonic acid (AA), on the activities of the ATP-sensitive K(+) (K(ATP)) channels of rat cardiac myocytes, using the inside-out patch-clamp technique. 2. In the presence of 100 microM cytoplasmic ATP, the K(ATP) channel open probability (P(o)) was increased by 240 +/- 60 % with 0.1 microM 11,12-EET and by 400 +/- 54 % with 5 microM 11,12-EET (n = 5-10, P < 0.05 vs. control), whereas neither 5 microM AA nor 5 microM 11,12-dihydroxyeicosatrienoic acid (DHET), which is the epoxide hydrolysis product of 11,12-EET, had any effect on P(o). 3. The half-maximal activating concentration (EC(50)) was 18.9 +/- 2.6 nM for 11,12-EET (n = 5) and 19.1 +/- 4.8 nM for 8,9-EET (n = 5, P = n.s. vs. 11,12-EET). Furthermore, 11,12-EET failed to alter the inhibition of K(ATP) channels by glyburide. 4. Application of 11,12-EET markedly decreased the channel sensitivity to cytoplasmic ATP. The half-maximal inhibitory concentration of ATP (IC(50)) was increased from 21.2 +/- 2.0 microM at baseline to 240 +/- 60 microM with 0.1 microM 11,12-EET (n = 5, P < 0.05 vs. control) and to 780 +/- 30 microM with 5 microM 11,12-EET (n = 11, P < 0.05 vs. control). 5. Increasing the ATP concentration increased the number of kinetically distinguishable closed states, promoting prolonged closure durations. 11,12-EET antagonized the effects of ATP on the kinetics of the K(ATP) channels in a dose- and voltage-dependent manner. 11,12-EET (1 microM) reduced the apparent association rate constant of ATP to the channel by 135-fold. 6. Application of 5 microM 11,12-EET resulted in hyperpolarization of the resting membrane potential in isolated cardiac myocytes, which could be blocked by glyburide. 7. These results suggest that EETs are potent activators of the cardiac K(ATP) channels, modulating channel behaviour by reducing the channel sensitivity to ATP. Thus, EETs could be important endogenous regulators of cardiac electrical excitability.

Indexed as

8,11,14-Eicosatrienoic AcidAdenosine TriphosphateAnimalsArachidonic AcidDose-Response Relationship, DrugElectrophysiologyGlyburideHeartKineticsMaleMembrane PotentialsMyocardiumPotassium Channel BlockersPotassium ChannelsRatsRats, Sprague-Dawley11,12-dihydroxy-5,8,14-eicosatrienoic acid11,12-epoxy-5,8,14-eicosatrienoic acid8,11,14-Eicosatrienoic Acid8,9-epoxyeicosatrienoic acidAdenosine TriphosphateArachidonic AcidGlyburidePotassium Channel BlockersPotassium Channels

Identifiers

PMID11744757
PMCPMC2278996
OpenAlexW2109776713

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.