Evidence map›Paper›PMID 27974315›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2017

Mechanisms of blood pressure salt sensitivity: new insights from mathematical modeling.

John S Clemmer, W Andrew Pruett, Thomas G Coleman, John E Hall, Robert L Hester

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Aging and sex differences in salt sensitivity of blood pressure.Clinical science (London, England : 1979) · 2025
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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 1 institution in 1 country.

John S ClemmerDepartment of Physiology and Biophysics, Center for Computational Medicine, University of Mississippi Medical Center, Jackson, Mississippi jclemmer@umc.edu.ORCID 0000-0003-2250-2960
W Andrew PruettDepartment of Physiology and Biophysics, Center for Computational Medicine, University of Mississippi Medical Center, Jackson, Mississippi.
Thomas G ColemanDepartment of Physiology and Biophysics, Center for Computational Medicine, University of Mississippi Medical Center, Jackson, Mississippi.
John E HallDepartment of Physiology and Biophysics, Center for Computational Medicine, University of Mississippi Medical Center, Jackson, Mississippi.
Robert L HesterDepartment of Physiology and Biophysics, Center for Computational Medicine, University of Mississippi Medical Center, Jackson, Mississippi.
University of Mississippi Medical Center · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI HESTER, ROBERT L · 1993 to 2018
$39.4M
Tracking and Evaluation CoreU54GM115428 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI HALL, JOHN E · 2016 to 2025
$38.2M
The role of leptin in autoimmune-associated hypertensionP20GM104357 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI TAYLOR, ERIN BASSFORD · 2013 to 2022
$23.4M
NHLBI NIH HHS P01 HL051971NIGMS NIH HHS P20 GM104357NIGMS NIH HHS U54 GM115428
6 · The paper itself

Abstract

Mathematical modeling is an important tool for understanding quantitative relationships among components of complex physiological systems and for testing competing hypotheses. We used HumMod, a large physiological model, to test hypotheses of blood pressure (BP) salt sensitivity. Systemic hemodynamics, renal, and neurohormonal responses to chronic changes in salt intake were examined during normal renal function, fixed low or high plasma angiotensin II (ANG II) levels, bilateral renal artery stenosis, increased renal sympathetic nerve activity (RSNA), and decreased nephron numbers. Simulations were run for 4 wk at salt intakes ranging from 30 to 1,000 mmol/day. Reducing functional kidney mass or fixing ANG II increased salt sensitivity. Salt sensitivity, associated with inability of ANG II to respond to changes in salt intake, occurred with smaller changes in renal blood flow but greater changes in glomerular filtration rate, renal sodium reabsorption, and total peripheral resistance (TPR). However, clamping TPR at normal or high levels had no major effect on salt sensitivity. There were no clear relationships between BP salt sensitivity and renal vascular resistance or extracellular fluid volume. Our robust mathematical model of cardiovascular, renal, endocrine, and sympathetic nervous system physiology supports the hypothesis that specific types of kidney dysfunction, associated with impaired regulation of ANG II or increased tubular sodium reabsorption, contribute to BP salt sensitivity. However, increased preglomerular resistance, increased RSNA, or inability to decrease TPR does not appear to influence salt sensitivity. This model provides a platform for testing competing concepts of long-term BP control during changes in salt intake.

Indexed as

Models, CardiovascularBaroreflexBlood PressureComputer SimulationHumansHypertensionKidneyOsmoregulationSodium Chloride, DietarySodium Chloride, Dietaryangiotensin IIcardiac outputhypertensionkidneyrenin-angiotensin systemsaltvascular resistance

Identifiers

PMID27974315
PMCPMC5407080
OpenAlexW2561819587

What OpenQuestion holds

Textmetadata
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.