Evidence map›Paper›PMID 15345750›Full record

Trial reportThe Journal of physiology2004

Inhibition of KATP channel activity augments baroreflex-mediated vasoconstriction in exercising human skeletal muscle.

David Melvin Keller, Shigehiko Ogoh, Shane Greene, A Olivencia-Yurvati, Peter B Raven

Open access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 60 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
    Trial
  2. Trial
  3. Endogenous muscarinic acetylcholine receptor signaling blunts αAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2025
    Article
  4. Review
  5. Sexual dimorphism in vascular ATP-sensitive KThe Journal of physiology · 2021
    Article
  6. Regulation of capillary hemodynamics by KPhysiological reports · 2021
    Article
  7. Vascular ATP-sensitive KThe Journal of physiology · 2020
    Article
  8. ATP-sensitive KRespiratory physiology & neurobiology · 2020
    Article
  9. Inhibition of NaThe Journal of physiology · 2018
    Article
  10. Article
  11. Article
  12. Vascular KRespiratory physiology & neurobiology · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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.

David Melvin KellerUniversity of North Texas Health Science Center at Fort Worth, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA. davidkeller@texashealth.org
Shigehiko Ogoh
Shane Greene
A Olivencia-Yurvati
Peter B Raven
University of North Texas Health Science Center · USUniversity of North Texas · US

Funding

ARTERIAL BAROREFLEX CONTROL OF BLOOD PRESSURE-- EXERCISER01HL045547 · NHLBI · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI RAVEN, PETER BERNARD · 1994 to 2006
$2.3M
NHLBI NIH HHS HL-045547NHLBI NIH HHS R01 HL045547
6 · The paper itself

Abstract

In the present investigation we examined the role of ATP-sensitive potassium (K(ATP)) channel activity in modulating carotid baroreflex (CBR)-induced vasoconstriction in the vasculature of the leg. The CBR control of mean arterial pressure (MAP) and leg vascular conductance (LVC) was determined in seven subjects (25 +/- 1 years, mean +/- S.E.M.) using the variable-pressure neck collar technique at rest and during one-legged knee extension exercise. The oral ingestion of glyburide (5 mg) did not change mean arterial pressure (MAP) at rest (86 versus 89 mmHg, P > 0.05), but did appear to increase MAP during exercise (87 versus 92 mmHg, P = 0.053). However, the CBR-MAP function curves were similar at rest before and after glyburide ingestion. The CBR-mediated decrease in LVC observed at rest (approximately 39%) was attenuated during exercise in the exercising leg (approximately 15%, P < 0.05). Oral glyburide ingestion partially restored CBR-mediated vasoconstriction in the exercising leg (approximately 40% restoration, P < 0.05) compared to control exercise. These findings indicate that K(ATP) channel activity modulates sympathetic vasoconstriction in humans and may prove to be an important mechanism by which functional sympatholysis operates in humans during exercise.

Indexed as

Adenosine TriphosphateAdultAnti-Arrhythmia AgentsBaroreflexCarotid BodyExerciseFemaleGlyburideHumansKneeMaleMuscle, SkeletalPotassium Channel BlockersPotassium ChannelsRestSympathetic Nervous SystemAdenosine TriphosphateAnti-Arrhythmia AgentsGlyburidePotassium Channel BlockersPotassium Channels

Identifiers

PMID15345750
PMCPMC1665325
OpenAlexW2149853348

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.