Evidence map›Paper›PMID 24555102›Full record

ArticleF1000Research2013

A computational analysis of the long-term regulation of arterial pressure.

Daniel A Beard, Klas H Pettersen, Brian E Carlson, Stig W Omholt, Scott M Bugenhagen

Open access · goldAbstract read
In one paragraph

Article in F1000Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

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  7. Computational models of cardiac hypertrophy.Progress in biophysics and molecular biology · 2021
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  8. Seven Mathematical Models of Hemorrhagic Shock.Computational and mathematical methods in medicine · 2021
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  12. A Simple Cardiovascular Model for the Study of Hemorrhagic Shock.Computational and mathematical methods in medicine · 2020
    Article
  13. Article
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  15. Article
  16. Clinical Applications of Patient-Specific Models: The Case for a Simple Approach.Journal of cardiovascular translational research · 2018
    Article
  17. Review
  18. Article
  19. Review
  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

5 authors at 4 institutions in 2 countries.

Daniel A BeardMolecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48105, USA.
Klas H PettersenDepartment of Mathematical and Technological Sciences, Norwegian University of Life Science, Oslo, Norway.
Brian E CarlsonDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Stig W OmholtCardiac Exercise Research Group, Department of Circulation and Medical Imaging, NTNU Norwegian University of Science and Technology, Trondheim, Norway.
Scott M BugenhagenDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Medical College of Wisconsin · USNorwegian University of Life Sciences · NONorwegian University of Science and Technology · NOUniversity of Michigan–Ann Arbor · US

Funding

The Virtual Physiological Rat ProjectP50GM094503 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BEARD, DANIEL A · 2011 to 2015
$11.6M
NIGMS NIH HHS P50 GM094503
6 · The paper itself

Abstract

The asserted dominant role of the kidneys in the chronic regulation of blood pressure and in the etiology of hypertension has been debated since the 1970s. At the center of the theory is the observation that the acute relationships between arterial pressure and urine production-the acute pressure-diuresis and pressure-natriuresis curves-physiologically adapt to perturbations in pressure and/or changes in the rate of salt and volume intake. These adaptations, modulated by various interacting neurohumoral mechanisms, result in chronic relationships between water and salt excretion and pressure that are much steeper than the acute relationships. While the view that renal function is the dominant controller of arterial pressure has been supported by computer models of the cardiovascular system known as the "Guyton-Coleman model", no unambiguous description of a computer model capturing chronic adaptation of acute renal function in blood pressure control has been presented. Here, such a model is developed with the goals of: 1. representing the relevant mechanisms in an identifiable mathematical model; 2. identifying model parameters using appropriate data; 3. validating model predictions in comparison to data; and 4. probing hypotheses regarding the long-term control of arterial pressure and the etiology of primary hypertension. The developed model reveals: long-term control of arterial blood pressure is primarily through the baroreflex arc and the renin-angiotensin system; and arterial stiffening provides a sufficient explanation for the etiology of primary hypertension associated with ageing. Furthermore, the model provides the first consistent explanation of the physiological response to chronic stimulation of the baroreflex.

Identifiers

PMID24555102
PMCPMC3886803
OpenAlexW2012187972

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.