Evidence map›Paper›PMID 24853828›Full record

ArticlePLoS computational biology2014

Arterial stiffening provides sufficient explanation for primary hypertension.

Klas H Pettersen, Scott M Bugenhagen, Javaid Nauman, Daniel A Beard, Stig W Omholt

Registry-linked trialAbstract read
In one paragraph

Article in PLoS computational biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06450327 (Resistant Hypertension An Open, Complicated), which is not on this map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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.

NCT06450327 recruitingnot on this mapstarted 2024, after this paper: background citation

Resistant Hypertension An Open, Complicated ("Cum Plicare") or Complex ("Cum Plexus")

TypeobservationalSponsorUniversity of Campinas, BrazilRan2024 to 2026Enrolled80ConditionsHypertension, Resistant HypertensionArmsThis is a cross-sectional observational study
3 · Its place in the literature

Who cites it

26 citing papers in PubMed.

  1. Article
  2. Article
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  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
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  11. Article
  12. Article
  13. Article
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  15. Article
  16. Review
  17. Article
  18. Rho Kinase Regulates Aortic Vascular Smooth Muscle Cell Stiffness Via Actin/SRF/Myocardin in Hypertension.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2017
    Article
  19. Review
  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

5 authors.

Klas H PettersenDepartment of Mathematical and Technological Sciences, Norwegian University of Life Sciences, Ås, Norway.
Scott M BugenhagenDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
Javaid NaumanDepartment of Circulation and Medical Imaging, Cardiac Exercise Research Group, NTNU Norwegian University of Science and Technology, Trondheim, Norway.
Daniel A BeardDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
Stig W OmholtDepartment of Circulation and Medical Imaging, Cardiac Exercise Research Group, NTNU Norwegian University of Science and Technology, Trondheim, Norway.

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 GM094503NIGMS NIH HHS P50-GM094503
6 · The paper itself

Abstract

Hypertension is one of the most common age-related chronic disorders, and by predisposing individuals for heart failure, stroke, and kidney disease, it is a major source of morbidity and mortality. Its etiology remains enigmatic despite intense research efforts over many decades. By use of empirically well-constrained computer models describing the coupled function of the baroreceptor reflex and mechanics of the circulatory system, we demonstrate quantitatively that arterial stiffening seems sufficient to explain age-related emergence of hypertension. Specifically, the empirically observed chronic changes in pulse pressure with age and the impaired capacity of hypertensive individuals to regulate short-term changes in blood pressure arise as emergent properties of the integrated system. The results are consistent with available experimental data from chemical and surgical manipulation of the cardio-vascular system. In contrast to widely held opinions, the results suggest that primary hypertension can be attributed to a mechanogenic etiology without challenging current conceptions of renal and sympathetic nervous system function.

Indexed as

BaroreflexBlood Flow VelocityBlood PressureModels, CardiovascularVascular StiffnessAnimalsArteriesComputer SimulationHumansHypertensionVascular Resistance

Identifiers

PMID24853828
PMCPMC4031054

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.