Evidence map›Paper›PMID 9169489›Full record

ArticleThe Journal of clinical investigation1997

ATP-sensitive potassium channels mediate contraction-induced attenuation of sympathetic vasoconstriction in rat skeletal muscle.

G D Thomas, J Hansen, R G Victor

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

41 citing papers in PubMed, 89 citations in OpenAlex.

  1. Intradermal administration of ATP does not mitigate tyramine-stimulated vasoconstriction in human skin.American journal of physiology. Regulatory, integrative and comparative physiology · 2010
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  8. KMicrovascular research · 2025
    Article
  9. Regulation of capillary hemodynamics by KPhysiological reports · 2021
    Article
  10. ATP-sensitive KRespiratory physiology & neurobiology · 2020
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  11. Article
  12. Article
  13. Article
  14. Vascular KRespiratory physiology & neurobiology · 2017
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  16. Article
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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.

G D ThomasDepartment of Internal Medicine, Molecular Cardiology Laboratories, The University of Texas Southwestern Medical Center, Dallas, Texas 75235, USA. gthomas@ryburn.swmed.edu
J Hansen
R G Victor
The University of Texas Southwestern Medical Center · US

Funding

Transcriptional control of muscle growth and remodelingP01HL006296 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI STULL, JAMES T · 1985 to 2006
$14.8M
NEURAL CONTROL OF SKELETAL MUSCLE METABOLISM IN HUMANSF05TW004949 · FIC · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI HANSEN, JIM · 1993 to 1994
–
FIC NIH HHS NIH-1-F05-TW04949-01NHLBI NIH HHS P01-HL-06296
6 · The paper itself

Abstract

Sympathetic vasoconstriction is sensitive to inhibition by metabolic events in contracting rat and human skeletal muscle, but the underlying cellular mechanisms are unknown. In rats, this inhibition involves mainly alpha2-adrenergic vasoconstriction, which relies heavily on Ca2+ influx through voltage-dependent Ca2+ channels. We therefore hypothesized that contraction-induced inhibition of sympathetic vasoconstriction is mediated by ATP-sensitive potassium (KATP) channels, a hyperpolarizing vasodilator mechanism that could be activated by some metabolic product(s) of skeletal muscle contraction. We tested this hypothesis in anesthetized rats by measuring femoral artery blood flow responses to lumbar sympathetic nerve stimulation or intraarterial hindlimb infusion of the specific alpha2-adrenergic agonist UK 14,304 during KATP channel activation with diazoxide in resting hindlimb and during KATP channel block with glibenclamide in contracting hindlimb. The major new findings are twofold. First, like muscle contraction, pharmacologic activation of KATP channels with diazoxide in resting hindlimb dose dependently attenuated the vasoconstrictor responses to either sympathetic nerve stimulation or intraarterial UK 14,304. Second, the large contraction-induced attenuation in sympathetic vasoconstriction elicited by nerve stimulation or UK 14,304 was partially reversed when the physiologic activation of KATP channels produced by muscle contraction was prevented with glibenclamide. We conclude that contraction-induced activation of KATP channels is a major mechanism underlying metabolic inhibition of sympathetic vasoconstriction in exercising skeletal muscle.

Indexed as

Adrenergic alpha-AgonistsAnimalsBrimonidine TartrateFemaleFemoral ArteryHumansMuscle ContractionMuscle, SkeletalPotassium ChannelsQuinoxalinesRatsRats, Sprague-DawleyRegional Blood FlowSympathetic Nervous SystemVasoconstrictionAdrenergic alpha-AgonistsBrimonidine TartratePotassium ChannelsQuinoxalines

Identifiers

PMID9169489
PMCPMC508105
OpenAlexW2022021204

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.