Evidence map›Paper›PMID 20299334›Full record

ArticleCardiovascular research2010

Caveolin-1 limits the contribution of BK(Ca) channel to EDHF-mediated arteriolar dilation: implications in diet-induced obesity.

Attila Feher, Ibolya Rutkai, Timea Beleznai, Zoltan Ungvari, Anna Csiszar, Istvan Edes, Zsolt Bagi

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 43 citations in OpenAlex.

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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

7 authors at 4 institutions in 3 countries.

Attila FeherDepartment of Physiology, New York Medical College, Valhalla, NY 10595, USA.
Ibolya Rutkai
Timea Beleznai
Zoltan Ungvari
Anna Csiszar
Istvan Edes
Zsolt Bagi
New York Medical College · USUniversity of Debrecen · HUUniversity of Oklahoma Health Sciences Center · USUniversity of Oxford · GB

Funding

PHS HHS 43023
6 · The paper itself

Abstract

aimsCaveolin-1 (Cav-1) interacts with large conductance Ca(2+)-activated potassium channels (BKCa) and likely exerts a negative regulatory effect on the channel activity. We investigated the role of Cav-1 in modulating BK(Ca) channel-mediated, endothelium-derived hyperpolarizing factor (EDHF)-dependent arteriolar dilation in normal condition and in an experimental model of obesity. METHODS AND

resultsIn isolated, pressurized (80 mmHg) gracilis muscle arterioles (approximately 100 microm) of Cav-1 knockout mice, acetylcholine (ACh)-induced, EDHF-mediated dilations were enhanced and were significantly reduced by the BK(Ca) channel inhibitor, iberiotoxin (IBTX), whereas IBTX had no effect on EDHF-mediated dilations in the wild-type mice. Dilations to the selective BK(Ca) channel opener, NS-1619 were augmented in the Cav-1 knockout mice. In high-fat diet-treated, obese rats ACh-induced coronary arteriolar dilations were preserved, whereas IBTX-sensitive, ACh-induced and also NS-1619-evoked vasodilations were augmented when compared with lean animals. In coronary arterioles of obese rats a reduced protein expression of Cav-1 was detected by western immunoblotting and immunohistochemistry. Moreover, in coronary arterioles of lean rats, disruption of caveolae with methyl-beta-cyclodextrin augmented IBTX-sensitive, ACh-induced, and also NS-1619-evoked dilations.

conclusionThus, under normal conditions, Cav-1 limits the contribution of the BK(Ca) channel to EDHF-mediated arteriolar dilation. In obesity, a reduced expression of Cav-1 leads to greater contribution of the BK(Ca) channel to EDHF-mediated response, which seems essential for maintained coronary dilation.

Indexed as

VasodilationAnimalsArteriolesBiological FactorsBlotting, WesternCaveolin 1Coronary VesselsDietary FatsDisease Models, AnimalDose-Response Relationship, DrugImmunohistochemistryLarge-Conductance Calcium-Activated Potassium ChannelsMiceMice, KnockoutMuscle, SkeletalObesityBiological FactorsCav1 protein, mouseCav1 protein, ratCaveolin 1Dietary Fatsendothelium-dependent hyperpolarization factorLarge-Conductance Calcium-Activated Potassium ChannelsPotassium Channel BlockersVasodilator Agents

Identifiers

PMID20299334
PMCPMC2920808
OpenAlexW2108655434

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.