Evidence map›Paper›PMID 30390036›Full record

ReviewHypertension research : official journal of the Japanese Society of Hypertension2019

Changing views on the common physiologic abnormality that mediates salt sensitivity and initiation of salt-induced hypertension: Japanese research underpinning the vasodysfunction theory of salt sensitivity.

Theodore W Kurtz, Stephen E DiCarlo, Michal Pravenec, R Curtis Morris

Abstract readReview
PubMed Publisher
In one paragraph

Review in Hypertension research : official journal of the Japanese Society of Hypertension, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Role of the microbiota in hypertension and antihypertensive drug metabolism.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Review
  7. Frequency of alcohol drinking modifies the association between salt intake and albuminuria: a 1-year observational study.Hypertension research : official journal of the Japanese Society of Hypertension · 2020
    Observational
  8. Review
  9. Article
  10. Sodium-induced inflammation-an invisible player in resistant hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2020
    Review
  11. Is alcohol drinking a key factor contributing to salt sensitivity?Journal of clinical hypertension (Greenwich, Conn.) · 2020
    Article
  12. 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 3 institutions in 2 countries.

Theodore W KurtzDepartment of Laboratory Medicine, University of California, San Francisco, School of Medicine, San Francisco, CA, 94107, USA. Ted.Kurtz@ucsf.edu.
Stephen E DiCarloDepartment of Physiology, Michigan State University, College of Osteopathic Medicine, East Lansing, MI, 48824, USA.
Michal PravenecInstitute of Physiology of the Czech Academy of Sciences, Prague, 14220, Czech Republic.
R Curtis MorrisDepartment of Medicine, University of California, San Francisco, School of Medicine, San Francisco, CA, 94143, USA.
University of California, San Francisco · USCzech Academy of Sciences, Institute of Physiology · CZMichigan 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

High-salt intake is one of the major dietary determinants of increased blood pressure and cardiovascular disease. Thus, there is scientific and medical interest in understanding the mechanistic abnormalities mediating the pressor effects of salt (salt sensitivity). According to historical theory, salt sensitivity stems from an impairment in renal function (referred to as "abnormal pressure natriuresis" or a "natriuretic handicap"), which causes salt-sensitive subjects to excrete a sodium load more slowly, and retain more of it than salt-resistant normotensive controls. However, this historical view has come under intense scrutiny because of growing awareness that in salt-sensitive subjects, acute salt loading does not usually induce greater increases in sodium balance and cardiac output than those induced by salt loading in salt-resistant normotensive controls. Here we highlight pioneering studies from Japan that challenge the historical thinking and provide insights into a contemporary theory of salt sensitivity termed the "vasodysfunction theory." According to this theory, initiation of salt-induced hypertension usually involves abnormal vascular resistance responses to increased salt intake, not greater renal retention of a salt load in salt-sensitive subjects than in normal subjects. By shifting the focus from the historical theory to a contemporary final common pathway for the pathogenesis of salt sensitivity, research from Japan is building the scientific foundation for more effective approaches to the prevention and treatment of salt-induced hypertension. Among the most promising approaches are dietary strategies for reducing the risk for salt-induced hypertension that do not depend on reducing salt consumption in the population.

Indexed as

Renal CirculationVascular ResistanceAnimalsArginineDietHumansHypertensionNitric OxideSalt StressSodiumSodium Chloride, DietaryArgininedimethylarginineNitric OxideSodiumSodium Chloride, Dietaryhypertensionsaltsalt sensitivitysodiumvasodysfunction

Identifiers

PMID30390036
OpenAlexW2898982269

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.