Evidence map›Paper›PMID 26371169›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2015

Neurotransmission to parasympathetic cardiac vagal neurons in the brain stem is altered with left ventricular hypertrophy-induced heart failure.

Edmund Cauley, Xin Wang, Jhansi Dyavanapalli, Ke Sun, Kara Garrott, Sarah Kuzmiak-Glancy, Matthew W Kay, David Mendelowitz

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Vagal GABAergic signaling in autonomic control of cardiometabolic function.American journal of physiology. Cell physiology · 2026
    Review
  3. Review
  4. Article
  5. Cardiac vagal motor neurons.Current opinion in neurobiology · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Novel approaches to restore parasympathetic activity to the heart in cardiorespiratory diseases.American journal of physiology. Heart and circulatory physiology · 2020
    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

8 authors at 1 institution in 1 country.

Edmund CauleyDepartment of Pharmacology and Physiology, The George Washington University, Washington, District of Columbia; and.
Xin WangDepartment of Pharmacology and Physiology, The George Washington University, Washington, District of Columbia; and.
Jhansi DyavanapalliDepartment of Pharmacology and Physiology, The George Washington University, Washington, District of Columbia; and.
Ke SunDepartment of Pharmacology and Physiology, The George Washington University, Washington, District of Columbia; and.
Kara GarrottDepartment of Biomedical Engineering, The George Washington University, Washington, District of Columbia.
Sarah Kuzmiak-GlancyDepartment of Biomedical Engineering, The George Washington University, Washington, District of Columbia.
Matthew W KayDepartment of Biomedical Engineering, The George Washington University, Washington, District of Columbia.
David MendelowitzDepartment of Pharmacology and Physiology, The George Washington University, Washington, District of Columbia; and dmendel@gwu.edu.
George Washington University · US

Funding

Nicotine Modulation of Parasympathetic Cardiac NeuronsR01HL072006 · NHLBI · GEORGE WASHINGTON UNIVERSITY · PI MENDELOWITZ, DAVID · 2003 to 2017
$5.4M
NEUROPHYSIOLOGY OF PARASYMPATHETIC CARDIAC NEURONSR01HL049965 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MENDELOWITZ, DAVID · 1998 to 2014
$4.6M
MECHANISM OF CARDIORESPIRATORY RHYTHM IN NEONATESR01HL059895 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MENDELOWITZ, DAVID · 1998 to 2013
$4.1M
Low flow reperfusion after acute myocardial ischemia: when too little is too muchR01HL095828 · NHLBI · GEORGE WASHINGTON UNIVERSITY · PI KAY, MATTHEW W. · 2010 to 2014
$1.6M
NEUROPHYSIOLOGY OF PARASYMPATHETIC CARDIAC NEURONSR29HL049965 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MENDELOWITZ, DAVID · 1993 to 1997
–
NHLBI NIH HHS HL-095828NHLBI NIH HHS HL-49965NHLBI NIH HHS HL-59895NHLBI NIH HHS HL-72006NHLBI NIH HHS R01 HL049965NHLBI NIH HHS R01 HL059895NHLBI NIH HHS R01 HL072006NHLBI NIH HHS R01 HL095828
6 · The paper itself

Abstract

Hypertension, cardiac hypertrophy, and heart failure (HF) are widespread and debilitating cardiovascular diseases that affect nearly 23 million people worldwide. A distinctive hallmark of these cardiovascular diseases is autonomic imbalance, with increased sympathetic activity and decreased parasympathetic vagal tone. Recent device-based approaches, such as implantable vagal stimulators that stimulate a multitude of visceral sensory and motor fibers in the vagus nerve, are being evaluated as new therapeutic approaches for these and other diseases. However, little is known about how parasympathetic activity to the heart is altered with these diseases, and this lack of knowledge is an obstacle in the goal of devising selective interventions that can target and selectively restore parasympathetic activity to the heart. To identify the changes that occur within the brain stem to diminish the parasympathetic cardiac activity, left ventricular hypertrophy was elicited in rats by aortic pressure overload using a transaortic constriction approach. Cardiac vagal neurons (CVNs) in the brain stem that generate parasympathetic activity to the heart were identified with a retrograde tracer and studied using patch-clamp electrophysiological recordings in vitro. Animals with left cardiac hypertrophy had diminished excitation of CVNs, which was mediated both by an augmented frequency of spontaneous inhibitory GABAergic neurotransmission (with no alteration of inhibitory glycinergic activity) as well as a diminished amplitude and frequency of excitatory neurotransmission to CVNs. Opportunities to alter these network pathways and neurotransmitter receptors provide future targets of intervention in the goal to restore parasympathetic activity and autonomic balance to the heart in cardiac hypertrophy and other cardiovascular diseases.

Indexed as

Synaptic TransmissionAnimalsBrain StemDisease Models, AnimalExcitatory Postsynaptic PotentialsGABAergic Neuronsgamma-Aminobutyric AcidGlutamic AcidGlycineHeartHeart FailureHypertrophy, Left VentricularIn Vitro TechniquesMaleNeural InhibitionNeural Pathwaysgamma-Aminobutyric AcidGlutamic AcidGlycineautonomiccardiac hypertrophyheart failureparasympatheticvagal

Identifiers

PMID26371169
PMCPMC4631536
OpenAlexW2107482106

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.