Evidence map›Paper›PMID 25344273›Full record

ReviewExperimental physiology2015

Autonomic control of the heart: going beyond the classical neurotransmitters.

Neil Herring

Open access · hybridAbstract readReview
In one paragraph

Review in Experimental physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.1field-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.

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

40 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
  2. Review
  3. The Evolving Features of Takotsubo Syndrome.Current cardiology reports · 2025
    Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Autonomic modulation of ventricular electrical activity: recent developments and clinical implications.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2021
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Neural control of cardiovascular function in black adults: implications for racial differences in autonomic regulation.American journal of physiology. Regulatory, integrative and comparative physiology · 2020
    Review
  19. Article
  20. Review
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

1 author at 1 institution in 1 country.

Neil HerringBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, OX1 3PT, UK.
University of Oxford · GB

Funding

British Heart Foundation FS/15/8/31155British Heart Foundation RE/08/004
6 · The paper itself

Abstract

NEW

findingsWhat is the topic of this review? This symposium report discusses the evidence for release of cardiac sympathetic cotransmitters in addition to noradrenaline. What advances does it highlight? It highlights the potential role of neuropeptide Y in reducing vagal neurotransmission and directly influencing ventricular myocyte excitability in the presence of β-receptor blockade. Acute myocardial infarction and congestive cardiac failure are characterized by high levels of cardiac sympathetic drive. In these conditions, sympathetic neurotransmitters such as neuropeptide Y (NPY) can be released in addition to noradrenaline, and plasma levels correlate with infarct size and mortality. Even in the presence of β-blockers, NPY is able to bind to its own receptors located on cholinergic ganglia and ventricular myocytes. In this symposium report, I review the evidence that NPY can inhibit acetylcholine release during vagus nerve stimulation and limit the subsequent bradycardia. I also present preliminary, as yet unpublished data, demonstrating that NPY may be pro-arrhythmic by directly influencing ventricular electrophysiology. Targeting NPY receptors pharmacologically may therefore be a useful therapeutic strategy both to reduce heart rate and to prevent arrhythmias in the setting of myocardial infarction and chronic heart failure. Such medications would be expected to act synergistically with β-blockers, angiotensin-converting enzyme inhibitors and implantable cardiac devices, such as defibrillators and vagus nerve stimulators.

Indexed as

AnimalsAutonomic Nervous SystemBlood PressureFeedback, PhysiologicalHeartHeart RateHumansModels, CardiovascularModels, NeurologicalNeurotransmitter AgentsNeurotransmitter Agents

Identifiers

PMID25344273
PMCPMC4405038
OpenAlexW2157827277

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.