Evidence map›Paper›PMID 9844020›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Impaired metabolic modulation of alpha-adrenergic vasoconstriction in dystrophin-deficient skeletal muscle.

G D Thomas, M Sander, K S Lau, P L Huang, J T Stull, R G Victor

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01502787 (Effects of Nebivolol Versus Metoprolol on Blood Flow Responses to Exercise and Angiotensin II in Hypertensive Patients), which is not on this map. Cited by 160 papers.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed
7.8field-weighted citation impact, top 2% 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.

NCT01502787 phase4completednot on this mapstarted 2009, after this paper: background citation

Effects of Nebivolol Versus Metoprolol on Blood Flow Responses to Exercise and Angiotensin II in Hypertensive Patients

TypeinterventionalSponsorUniversity of Texas Southwestern Medical CenterRan2009 to 2013Enrolled46ConditionsHypertensionArmsMetoprolol succinate, Nebivolol, Forearm blood flow, Microneurography, Rhythmic handgrip exercise
3 · Its place in the literature

Who cites it

160 citing papers in PubMed, 372 citations in OpenAlex.

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  16. Mechanisms of reduced myocardial energetics of the dystrophic heart.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  17. Review
  18. Review
  19. Pathophysiology and Management of Fatigue in Neuromuscular Diseases.International journal of molecular sciences · 2023
    Review
  20. Review

100 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

G D ThomasDepartment of Internal Medicine, Hypertension Division, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235, USA. gthom1@mednet.swmed.edu
M Sander
K S Lau
P L Huang
J T Stull
R G Victor
Massachusetts General Hospital · USHarvard University · USSouthwestern Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

Transcriptional control of muscle growth and remodelingP01HL006296 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI BASSEL-DUBY, RHONDA · 1985 to 2006
$14.8M
NHLBI NIH HHS P01 HL006296NHLBI NIH HHS P01-HL-06296
6 · The paper itself

Abstract

The neuronal isoform of nitric oxide synthase (nNOS) is highly expressed in mammalian skeletal muscle, but its functional role has not been defined. NO has been implicated in the local metabolic regulation of blood flow in contracting skeletal muscle in part by antagonizing sympathetic vasoconstriction. We therefore hypothesized that nNOS in skeletal muscle is the source of the NO mediating the inhibition of sympathetic vasoconstriction in contracting muscle. In the mdx mouse, a model of Duchenne muscular dystrophy in which dystrophin deficiency results in greatly reduced expression of nNOS in skeletal muscle, we found that the normal ability of skeletal muscle contraction to attenuate alpha-adrenergic vasoconstriction is defective. Similar results were obtained in mutant mice that lack the gene encoding nNOS. Together these data suggest a specific role for nNOS in the local metabolic inhibition of alpha-adrenergic vasoconstriction in active skeletal muscle.

Indexed as

AnimalsDystrophinMaleMiceMice, Inbred C57BLMuscle, SkeletalMuscular Dystrophy, AnimalReceptors, Adrenergic, alphaVasoconstrictionDystrophinReceptors, Adrenergic, alpha

Identifiers

PMID9844020
PMCPMC24580
OpenAlexW2052928078

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.