Evidence map›Paper›PMID 11927694›Full record

Trial reportThe Journal of physiology2002

Nitric oxide-dependent modulation of sympathetic neural control of oxygenation in exercising human skeletal muscle.

Bahman Chavoshan, Mikael Sander, Troy E Sybert, Jim Hansen, Ronald G Victor, Gail D Thomas

Registry-linked trialOpen access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in The Journal of physiology, 2002. 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 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

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4 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 1 institution in 1 country.

Bahman ChavoshanDepartment of Internal Medicine, Hypertension Division, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.
Mikael Sander
Troy E Sybert
Jim Hansen
Ronald G Victor
Gail D Thomas
The 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
TRAINING IN CARDIOVASCULAR RESEARCHT32HL007360 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 1985 to 2012
$11.8M
NHLBI NIH HHS HL06296NHLBI NIH HHS HL07360NHLBI NIH HHS P01 HL006296NHLBI NIH HHS T32 HL007360
6 · The paper itself

Abstract

Nitric oxide (NO) attenuates alpha-adrenergic vasoconstriction in contracting rodent skeletal muscle, but it is unclear if NO plays a similar role in human muscle. We therefore hypothesized that in humans, NO produced in exercising skeletal muscle blunts the vasoconstrictor response to sympathetic activation. We assessed vasoconstrictor responses in the microcirculation of human forearm muscle using near-infrared spectroscopy to measure decreases in muscle oxygenation during reflex sympathetic activation evoked by lower body negative pressure (LBNP). Experiments were performed before and after NO synthase inhibition produced by systemic infusion of N(G)-nitro-L-arginine methyl ester (L-NAME). Before L-NAME, LBNP at -20 mmHg decreased muscle oxygenation by 20 +/- 2 % in resting forearm and by 2 +/- 3 % in exercising forearm (n = 20), demonstrating metabolic modulation of sympathetic vasoconstriction. As expected, L-NAME increased mean arterial pressure by 17 +/- 3 mmHg, leading to baroreflex-mediated suppression of baseline muscle sympathetic nerve activity (SNA). The increment in muscle SNA in response to LBNP at -20 mmHg also was attenuated after L-NAME (before, +14 +/- 2; after, +8 +/- 1 bursts min(-1); n = 6), but this effect of L-NAME was counteracted by increasing LBNP to -40 mmHg (+19 +/- 2 bursts min(-1)). After L-NAME, LBNP at -20 mmHg decreased muscle oxygenation similarly in resting (-11 +/- 3 %) and exercising (-10 +/- 2 %) forearm (n = 12). Likewise, LBNP at -40 mmHg decreased muscle oxygenation both in resting (-19 +/- 4 %) and exercising (-21 +/- 5 %) forearm (n = 8). These data advance the hypothesis that NO plays an important role in modulating sympathetic vasoconstriction in the microcirculation of exercising muscle, because such modulation is abrogated by NO synthase inhibition with L-NAME.

Indexed as

AdultAnesthesiaAnimalsBaroreflexConsciousnessElectric StimulationEnzyme InhibitorsFemaleForearmHumansLower Body Negative PressureMaleMuscle ContractionMuscle, SkeletalNG-Nitroarginine Methyl EsterNitric OxideEnzyme InhibitorsNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide Synthase

Identifiers

PMID11927694
PMCPMC2290221
OpenAlexW2021489239

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.