Evidence map›Paper›PMID 23970531›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2013

No independent, but an interactive, role of calcium-activated potassium channels in human cutaneous active vasodilation.

Vienna E Brunt, Naoto Fujii, Christopher T Minson

Open access · greenAbstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.3field-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

23 citing papers in PubMed, 45 citations in OpenAlex.

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  8. Separate and combined effects of KAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2019
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  15. K+ channel mechanisms underlying cholinergic cutaneous vasodilation and sweating in young humans: roles of KCa, KATP, and KV channels?American journal of physiology. Regulatory, integrative and comparative physiology · 2016
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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

3 authors at 1 institution in 1 country.

Vienna E BruntDepartment of Human Physiology, University of Oregon, Eugene, Oregon.
Naoto Fujii
Christopher T Minson
University of Oregon · US

Funding

Progesterone and Vascular Function in WomenR01HL081671 · NHLBI · UNIVERSITY OF OREGON · PI MINSON, CHRISTOPHER TODD · 2008 to 2011
$1.3M
NHLBI NIH HHS HL-081671
6 · The paper itself

Abstract

In human cutaneous microvasculature, endothelium-derived hyperpolarizing factors (EDHFs) account for a large portion of vasodilation associated with local stimuli. Thus we sought to determine the role of EDHFs in active vasodilation (AVD) to passive heating in two protocols. Whole body heating was achieved using water-perfused suits (core temperature increase of 0.8-1.0°C), and skin blood flow was measured using laser-Doppler flowmetry. In the first protocol, four sites were perfused continuously via microdialysis with: 1) control; 2) tetraethylammonium (TEA) to block calcium-activated potassium (KCa) channels, and thus the actions of EDHFs; 3) N-nitro-l-arginine methyl ester (l-NAME) to inhibit nitric oxide synthase (NOS); and 4) TEA + l-NAME (n = 8). Data are presented as percent maximal cutaneous vascular conductance (CVC). TEA had no effect on AVD (CVC during heated plateau: control 57.4 ± 4.9% vs. TEA 63.2 ± 5.2%, P = 0.27), indicating EDHFs are not obligatory. l-NAME attenuated plateau CVC to 33.7 ± 5.4% (P < 0.01 vs. control); while TEA + l-NAME augmented plateau CVC compared with l-NAME alone (49.7 ± 5.3%, P = 0.02). From these data, it appears combined blockade of EDHFs and NOS necessitates dilation through other means, possibly through inward rectifier (KIR) and/or ATP-sensitive (KATP) potassium channels. To test this second hypothesis, we measured AVD at the following sites (n = 8): 1) control, 2) l-NAME, 3) l-NAME + TEA, and 4) l-NAME + TEA + barium chloride (BaCl2; KIR and KATP blocker). The addition of BaCl2 to l-NAME + TEA reduced plateau CVC to 32.7 ± 6.6% (P = 0.02 vs. l-NAME + TEA), which did not differ from the l-NAME site. These data combined demonstrate a complex interplay between vasodilatory pathways, with cross-talk between NO, KCa channels, and KIR and/or KATP channels.

Indexed as

AdultBiological FactorsFemaleHot TemperatureHumansLaser-Doppler FlowmetryMaleMicrodialysisNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthasePotassium Channels, Calcium-ActivatedRegional Blood FlowSkinTetraethylammoniumVasodilationBiological Factorsendothelium-dependent hyperpolarization factorNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthasePotassium Channels, Calcium-ActivatedTetraethylammoniumendothelium-derived hyperpolarizing factorsinward rectifier potassium channelsnitric oxidethermoregulationwhole body heating

Identifiers

PMID23970531
PMCPMC3841827
OpenAlexW2001644667

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.