Evidence map›Paper›PMID 24816260›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2014

Exercise training improves functional sympatholysis in spontaneously hypertensive rats through a nitric oxide-dependent mechanism.

Masaki Mizuno, Gary A Iwamoto, Wanpen Vongpatanasin, Jere H Mitchell, Scott A Smith

Registry-linked trialAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02664519 (Mechanisms of Muscle Blood Flow Dysregulation and Exercise Intolerance in Chronic Kidney Disease), which is not on this map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.5field-weighted citation impact, top 5% 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.

NCT02664519 naterminatednot on this mapstarted 2016, after this paper: background citation

Mechanisms of Muscle Blood Flow Dysregulation and Exercise Intolerance in Chronic Kidney Disease

TypeinterventionalSponsorUniversity of Texas Southwestern Medical CenterRan2016 to 2021Enrolled32ConditionsChronic Kidney DiseaseArmsForearm exercise training
3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 46 citations in OpenAlex.

  1. Trial
  2. Obligatory neural feedback control of exercise cardiorespiratory function and performance.Journal of applied physiology (Bethesda, Md. : 1985) · 2025
    Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Sex differences in sympathetic vasoconstrictor responsiveness and sympatholysis.Journal of applied physiology (Bethesda, Md. : 1985) · 2017
    Article
  12. Article
  13. Article
  14. Exercise, the Brain, and Hypertension.Current hypertension reports · 2015
    Review
  15. Dynamic exercise training prevents exercise pressor reflex overactivity in spontaneously hypertensive rats.American journal of physiology. Heart and circulatory physiology · 2015
    Article
  16. Article
  17. Review
  18. Article
  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 1 institution in 1 country.

Masaki MizunoDepartment of Health Care Sciences, University of Texas Southwestern Medical Center, Dallas, Texas;
Gary A IwamotoDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas;
Wanpen VongpatanasinDepartment of Hypertension Section University of Texas Southwestern Medical Center, Dallas, Texas; and Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas.
Jere H MitchellDivision of Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas.
Scott A SmithDepartment of Health Care Sciences, University of Texas Southwestern Medical Center, Dallas, Texas; Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas scott.smith@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · US

Funding

The Role of Aldosterone on Augmented Exercise Pressor Reflex in HypertensionR01HL113738 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI VONGPATANASIN, WANPEN · 2013 to 2016
$2.2M
Mechanisms of Exercise Pressor Reflex Overactivity in HypertensionR01HL088422 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI SMITH, SCOTT A · 2008 to 2012
$2.0M
NHLBI NIH HHS HL-088422NHLBI NIH HHS HL-113738
6 · The paper itself

Abstract

Functional sympatholysis is impaired in hypertensive animals and patients. Exercise training (ET) improves functional sympatholysis through a nitric oxide (NO)-dependent mechanism in normotensive rats. However, whether ET has similar physiological benefits in hypertension remains to be elucidated. Thus we tested the hypothesis that the impairment in functional sympatholysis in hypertension is reversed by ET through a NO-dependent mechanism. In untrained normotensive Wistar-Kyoto rats (WKYUT; n = 13), untrained spontaneously hypertensive rats (SHRUT; n = 13), and exercise-trained SHR (SHRET; n = 6), changes in femoral vascular conductance (FVC) were examined during lumbar sympathetic nerve stimulation (1, 2.5, and 5 Hz) at rest and during muscle contraction. The magnitude of functional sympatholysis (Δ%FVC = Δ%FVC muscle contraction - Δ%FVC rest) in SHRUT was significantly lower than WKYUT (1 Hz: -2 ± 4 vs. 13 ± 3%; 2.5 Hz: 9 ± 3 vs. 21 ± 3%; and 5 Hz: 12 ± 3 vs. 26 ± 3%, respectively; P < 0.05). Three months of voluntary wheel running significantly increased maximal oxygen uptake in SHRET compared with nontrained SHRUT (78 ± 6 vs. 62 ± 4 ml·kg(-1)·min(-1), respectively; P < 0.05) and restored the magnitude of functional sympatholysis in SHRET (1 Hz: 9 ± 2%; 2.5 Hz: 20 ± 4%; and 5 Hz: 34 ± 5%). Blockade of NO synthase (NOS) by N(G)-nitro-l-arginine methyl ester attenuated functional sympatholysis in WKYUT but not SHRUT. Furthermore, NOS inhibition significantly diminished the improvements in functional sympatholysis in SHRET. These data demonstrate that impairments in functional sympatholysis are normalized via a NO mechanism by voluntary wheel running in hypertensive rats.

Indexed as

Exercise TherapyVasoconstrictionAnimalsBlood PressureDisease Models, AnimalElectric StimulationEnzyme InhibitorsFemoral ArteryHypertensionMaleMuscle ContractionMuscle, SkeletalNitric OxideNitric Oxide SynthaseOxygen ConsumptionRatsEnzyme InhibitorsNitric OxideNitric Oxide Synthaseblood flowblood pressuremuscle contractionvascular conductancevoluntary running

Identifiers

PMID24816260
PMCPMC4101645
OpenAlexW2095033564

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.