Evidence map›Paper›PMID 25698230›Full record

ArticleJournal of theoretical biology2015

Modelling the vascular response to sympathetic postganglionic nerve activity.

Linford J B Briant, Julian F R Paton, Anthony E Pickering, Alan R Champneys

Open access · hybridAbstract read
In one paragraph

Article in Journal of theoretical biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Untangling Peripheral Sympathetic Neurocircuits.Frontiers in cardiovascular medicine · 2022
    Article
  6. Review
  7. Article
  8. Article
  9. 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

4 authors at 2 institutions in 1 country.

Linford J B BriantSchool of Physiology & Pharmacology, Medical Sciences Building, University Walk, University of Bristol, Bristol BS8 1TD, UK; Department of Engineering Mathematics, Merchant Venturers Building, Woodland Road, University of Bristol, Bristol BS8 1UB, UK.
Julian F R PatonSchool of Physiology & Pharmacology, Medical Sciences Building, University Walk, University of Bristol, Bristol BS8 1TD, UK.
Anthony E PickeringSchool of Physiology & Pharmacology, Medical Sciences Building, University Walk, University of Bristol, Bristol BS8 1TD, UK; Department of Anaesthesia, University Hospitals Bristol, Bristol BS2 8HW, UK.
Alan R ChampneysDepartment of Engineering Mathematics, Merchant Venturers Building, Woodland Road, University of Bristol, Bristol BS8 1UB, UK. Electronic address: A.R.Champneys@Bristol.ac.uk.
University of Bristol · GBUniversity Hospitals Bristol NHS Foundation Trust · GB

Funding

British Heart Foundation PG/06/084British Heart Foundation RG/12/6/29670Wellcome Trust 088373
6 · The paper itself

Abstract

This paper explores the influence of burst properties of the sympathetic nervous system on arterial contractility. Specifically, a mathematical model is constructed of the pathway from action potential generation in a sympathetic postganglionic neurone to contraction of an arterial smooth muscle cell. The differential equation model is a synthesis of models of the individual physiological processes, and is shown to be consistent with physiological data. The model is found to be unresponsive to tonic (regular) stimulation at typical frequencies recorded in sympathetic efferents. However, when stimulated at the same average frequency, but with repetitive respiratory-modulated burst patterns, it produces marked contractions. Moreover, the contractile force produced is found to be highly dependent on the number of spikes in each burst. In particular, when the model is driven by preganglionic spike trains recorded from wild-type and spontaneously hypertensive rats (which have increased spiking during each burst) the contractile force was found to be 10-fold greater in the hypertensive case. An explanation is provided in terms of the summative increased release of noradrenaline. Furthermore, the results suggest the marked effect that hypertensive spike trains had on smooth muscle cell tone can provide a significant contribution to the pathology of hypertension.

Indexed as

Models, CardiovascularAnimalsCalciumGTP-Binding ProteinsInositol 1,4,5-TrisphosphateMuscle ContractionMyocytes, Smooth MuscleNeuronsNorepinephrineRats, Inbred SHRReproducibility of ResultsSignal TransductionSympathetic Nervous SystemCalciumGTP-Binding ProteinsInositol 1,4,5-TrisphosphateNorepinephrineBurstingCalcium dynamicsHypertensionNeurone dynamicsSympathetic nervous system

Identifiers

PMID25698230
PMCPMC4386929
OpenAlexW2072647461

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.