Evidence map›Paper›PMID 28637271›Full record

ArticleAmerican journal of hypertension2016

Logical Issues With the Pressure Natriuresis Theory of Chronic Hypertension.

Theodore W Kurtz, Stephen E DiCarlo, R Curtis Morris

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in American journal of hypertension, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.5field-weighted citation impact, top 11% 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, 19 citations in OpenAlex.

  1. Acute effects of salt on blood pressure are mediated by serum osmolality.Journal of clinical hypertension (Greenwich, Conn.) · 2018
    Trial
  2. Review
  3. Seven Mathematical Models of Hemorrhagic Shock.Computational and mathematical methods in medicine · 2021
    Review
  4. Article
  5. Review
  6. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Theodore W KurtzDepartment of Laboratory Medicine, University of California, San Francisco, California, USA.
Stephen E DiCarloDepartment of Physiology, Wayne State University, Detroit, Michigan, USA.
R Curtis MorrisDepartment of Medicine, University of California, San Francisco, California, USA.
University of California, San Francisco · USWayne State University · US

Funding

ZD1839 FOR MALIGNANT ASTROCYTOMA OR GLIOBLASTOMA AND MENINGIOMAM01RR000079 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KESSLER, DAVID A · 1985 to 2006
$26.0M
SELECTIVE SODIUM-SENSITIVITY IN SALT-SENSITIVE BLACKSR01HL064230 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MORRIS, RALPH CURTIS · 2000 to 2006
$2.1M
NCRR NIH HHS M01 RR000079NHLBI NIH HHS R01 HL064230
6 · The paper itself

Abstract

The term "abnormal pressure natriuresis" refers to a subnormal effect of a given level of blood pressure (BP) on sodium excretion. It is widely believed that abnormal pressure natriuresis causes an initial increase in BP to be sustained. We refer to this view as the "pressure natriuresis theory of chronic hypertension." The proponents of the theory contend that all forms of chronic hypertension are sustained by abnormal pressure natriuresis, irrespective of how hypertension is initiated. This theory would appear to follow from "the three laws of long-term arterial pressure regulation" stated by Guyton and Coleman more than 3 decades ago. These "laws" articulate the concept that for a given level of salt intake, the relationship between arterial pressure and sodium excretion determines the chronic level of BP. Here, we review and examine the recent assertion by Beard that these "laws" of long-term BP control amount to nothing more than a series of tautologies. Our analysis supports Beard's assertion, and also indicates that contemporary investigators often use tautological reasoning in support of the pressure natriuresis theory of chronic hypertension. Although the theory itself is not a tautology, it does not appear to be testable because it holds that abnormal pressure natriuresis causes salt-induced hypertension to be sustained through abnormal increases in cardiac output that are too small to be detected.

Indexed as

AnimalsBlood PressureChronic DiseaseHumansHypertensionNatriuresisPressureblood pressurehypertensionkidneypressure natriuresissaltsalt resistancesalt sensitivitysodium.

Identifiers

PMID28637271
PMCPMC5353574
OpenAlexW2586724690

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.