Evidence map›Paper›PMID 25376899›Full record

ReviewNephron. Physiology2014

Mineralocorticoid-induced sodium appetite and renal salt retention: evidence for common signaling and effector mechanisms.

Yiling Fu, Volker Vallon

Open access · bronzeAbstract readReview
In one paragraph

Review in Nephron. Physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
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  13. Article
  14. Review
  15. Review
  16. Article
  17. Understanding the Two Faces of Low-Salt Intake.Current hypertension reports · 2017
    Review
  18. Gastrointestinal-Renal Axis: Role in the Regulation of Blood Pressure.Journal of the American Heart Association · 2017
    Review
  19. Serum and Glucocorticoid Regulated Kinase 1 in Sodium Homeostasis.International journal of molecular sciences · 2016
    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

2 authors at 2 institutions in 2 countries.

Yiling FuDepartment of Medicine, University of California San Diego, La Jolla, Calif., USA.
Volker Vallon
Karger Publishers (Switzerland) · CHUniversity of California, San Diego · US

Funding

UAB-UCSD O'Brien Core Center for Acute Kidney Injury ResearchP30DK079337 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AGARWAL, ANUPAM · 2008 to 2022
$18.3M
GLOMERULAR AND TUBULAR FUNCTION IN THE DIABETIC KIDNEYR01DK056248 · NIDDK · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI THOMSON, SCOTT CULVER · 1999 to 2014
$4.6M
Blood Pressure Regulation by OAT3R01HL094728 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ERALY, SATISH A, VALLON, VOLKER · 2010 to 2014
$1.9M
NHLBI NIH HHS R01 HL094728NHLBI NIH HHS R01HL94728NIDDK NIH HHS NIH-P30DK079337NIDDK NIH HHS P30 DK079337NIDDK NIH HHS R01 DK056248NIDDK NIH HHS R01DK56248
6 · The paper itself

Abstract

An increase in renal sodium chloride (salt) retention and an increase in sodium appetite are the body's responses to salt restriction or depletion in order to restore salt balance. Renal salt retention and increased sodium appetite can also be maladaptive and sustain the pathophysiology in conditions like salt-sensitive hypertension and chronic heart failure. Here we review the central role of the mineralocorticoid aldosterone in both the increase in renal salt reabsorption and sodium appetite. We discuss the working hypothesis that aldosterone activates similar signaling and effector mechanisms in the kidney and brain, including the mineralocorticoid receptor, the serum- and glucocorticoid-induced kinase SGK1, the ubiquitin ligase NEDD4-2, and the epithelial sodium channel ENaC. The latter also mediates the gustatory salt sensing in the tongue, which is required for the manifestation of increased salt intake. Effects of aldosterone on both the brain and kidney synergize with the effects of angiotensin II. Thus, mineralocorticoids appear to induce similar molecular pathways in the kidney, brain, and possibly tongue, which could provide opportunities for more effective therapeutic interventions. Inhibition of renal salt reabsorption is compensated by stimulation of salt appetite and vice versa; targeting both mechanisms should be more effective. Inhibiting the arousal to consume salty food may improve a patient's compliance to reducing salt intake. While a better understanding of the molecular mechanisms is needed and will provide new therapeutic options, current pharmacological interventions that target both salt retention and sodium appetite include mineralocorticoid receptor antagonists and potentially inhibitors of angiotensin II and ENaC.

Indexed as

AldosteroneAngiotensin IIAnimalsAppetiteBlood PressureEpithelial Sodium ChannelsHumansHypertensionKidneyMineralocorticoid Receptor AntagonistsMineralocorticoidsReceptors, MineralocorticoidSignal TransductionSodium ChlorideWater-Electrolyte BalanceAldosteroneAngiotensin IIEpithelial Sodium ChannelsMineralocorticoid Receptor AntagonistsMineralocorticoidsReceptors, MineralocorticoidSodium Chloride

Identifiers

PMID25376899
PMCPMC4275376
OpenAlexW1979751404

What OpenQuestion holds

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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.