Evidence map›Paper›PMID 18385465›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2008

Exercise training normalizes enhanced glutamate-mediated sympathetic activation from the PVN in heart failure.

Allison C Kleiber, Hong Zheng, Harold D Schultz, Jacob D Peuler, Kaushik P Patel

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
19.3field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
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  4. Exercise in treatment-resistant hypertension. A natural neuromodulation therapy?Hypertension research : official journal of the Japanese Society of Hypertension · 2023
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2 more citing papers are in PubMed but not listed here.

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 2 countries.

Allison C KleiberDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, 985850 Nebraska Medical Center, Omaha, NE 68198-5850, USA.
Hong Zheng
Harold D Schultz
Jacob D Peuler
Kaushik P Patel
Laboratoire d’immunologie intégrative du cancer · FRUniversity of Nebraska Medical Center · US

Funding

The Role of Excitatory Input into the PVN on Increased Sympathetic Drive in HeartP01HL062222 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI CORNISH, KURTIS G · 1999 to 2019
$32.2M
NHLBI NIH HHS HL 62222NHLBI NIH HHS P01 HL062222
6 · The paper itself

Abstract

Exercise training (ExT) normalizes the increased sympathetic outflow in heart failure (HF), but the mechanisms are not known. We hypothesized that ExT would normalize the augmented glutamatergic mechanisms mediated by N-methyl-d-aspartic acid (NMDA) receptors within the paraventricular nucleus (PVN) that occur with HF. Four groups of rats were used: 1) sham-operated (Sham) sedentary (Sed), 2) Sham ExT, 3) HF Sed, and 4) HF ExT. HF was induced by left coronary artery ligation, and ExT consisted of 3 wk of treadmill running. In alpha-chloralose-urethane-anesthetized rats, the increase in renal sympathetic nerve activity in response to the highest dose of NMDA (200 pmol) injected into the PVN in the HF Sed group was approximately twice that of the Sham Sed group. In the HF ExT group the response was not different from the Sham Sed and Sham ExT groups. Relative NMDA NR1 receptor subunit mRNA expression was 63% higher in the HF Sed group compared with the Sham Sed group but in the HF ExT group was not different from the Sham Sed and Sham ExT groups. NR1 receptor subunit protein expression was increased 87% in the HF Sed group compared with the Sham Sed group but in the HF ExT group was not significantly different from the Sham Sed and Sham ExT groups. Thus one mechanism by which ExT alleviates elevated sympathetic outflow in HF may be through normalization of glutamatergic mechanisms within the PVN.

Indexed as

AnimalsExcitatory Amino Acid AgonistsGlutamatesHeart FailureKidneyMaleN-MethylaspartateParaventricular Hypothalamic NucleusPhysical Conditioning, AnimalRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateRNA, MessengerSympathetic Nervous SystemExcitatory Amino Acid AgonistsGlutamatesN-MethylaspartateReceptors, N-Methyl-D-AspartateRNA, Messenger

Identifiers

PMID18385465
PMCPMC4107908
OpenAlexW2071319392

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.