Evidence map›Paper›PMID 28533325›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2017

Physiologic regulation of heart rate and blood pressure involves connexin 36-containing gap junctions.

Varinder K Lall, Gareth Bruce, Larysa Voytenko, Mark Drinkhill, Kerstin Wellershaus, Klaus Willecke, Jim Deuchars, Susan A Deuchars

Open access · hybridAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Peripheral Gating of Nociception Investigated with a Decerebrate, Arterially Perfused Preparation of the Rat.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  2. Article
  3. Article
  4. The Roles of Calmodulin and CaMKII in Cx36 Plasticity.International journal of molecular sciences · 2021
    Review
  5. Article
  6. 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

8 authors at 2 institutions in 2 countries.

Varinder K LallFaculty of Biological Sciences, School of Biomedical Sciences, University of Leeds, Leeds, United Kingdom.
Gareth BruceFaculty of Biological Sciences, School of Biomedical Sciences, University of Leeds, Leeds, United Kingdom.
Larysa VoytenkoFaculty of Biological Sciences, School of Biomedical Sciences, University of Leeds, Leeds, United Kingdom.
Mark DrinkhillDivision of Cardiovascular and Diabetes Research, Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, United Kingdom.
Kerstin WellershausLife and Medical Sciences Institute (LIMES), University of Bonn, Bonn, Germany.
Klaus WilleckeLife and Medical Sciences Institute (LIMES), University of Bonn, Bonn, Germany.
Jim DeucharsFaculty of Biological Sciences, School of Biomedical Sciences, University of Leeds, Leeds, United Kingdom.
Susan A DeucharsFaculty of Biological Sciences, School of Biomedical Sciences, University of Leeds, Leeds, United Kingdom; s.a.deuchars@leeds.ac.uk.
University of Leeds · GBUniversity of Bonn · DE

Funding

Biotechnology and Biological Sciences Research Council BB/E001831/1British Heart Foundation PG/08/120/26338Wellcome TrustWellcome Trust WT093072MA
6 · The paper itself

Abstract

Chronically elevated sympathetic nervous activity underlies many cardiovascular diseases. Elucidating the mechanisms contributing to sympathetic nervous system output may reveal new avenues of treatment. The contribution of the gap junctional protein connexin 36 (Cx36) to the regulation of sympathetic activity and thus blood pressure and heart rate was determined using a mouse with specific genetic deletion of Cx36. Ablation of the Cx36 protein was confirmed in sympathetic preganglionic neurons of Cx36-knockout (KO) mice. Telemetric analysis from conscious Cx36 KO mice revealed higher variance in heart rate and blood pressure during rest and activity compared to wild-type (WT) mice, and smaller responses to chemoreceptor activation when anesthetized. In the working heart-brain stem preparation of the Cx36-KO mouse, respiratory-coupled sympathetic nerve discharge was attenuated and responses to chemoreceptor stimulation and noxious stimulation were blunted compared to WT mice. Using whole cell patch recordings, sympathetic preganglionic neurons in spinal cord slices of Cx36-KO mice displayed lower levels of spikelet activity compared to WT mice, indicating reduced gap junction coupling between neurons. Cx36 deletion therefore disrupts normal regulation of sympathetic outflow with effects on cardiovascular parameters.-Lall, V. K., Bruce, G., Voytenko, L., Drinkhill, M., Wellershaus, K., Willecke, K., Deuchars, J., Deuchars, S. A. Physiologic regulation of heart rate and blood pressure involves connexin 36-containing gap junctions.

Indexed as

AnimalsBlood PressureChemoreceptor CellsConnexinsElectrophysiological PhenomenaFemaleGap Junction delta-2 ProteinGap JunctionsHeart RateMaleMiceMice, KnockoutSodium CyanideSympathetic Nervous SystemConnexinsGap Junction delta-2 ProteinSodium Cyanidecardiovascularknockout modelsspinal cordsympathetic

Identifiers

PMID28533325
PMCPMC5566179
OpenAlexW2614081373

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.