Evidence map›Paper›PMID 24535442›Full record

ReviewThe Journal of physiology2014

Glucocorticoids and renal Na+ transport: implications for hypertension and salt sensitivity.

Robert W Hunter, Jessica R Ivy, Matthew A Bailey

Open access · hybridAbstract readReview
In one paragraph

Review in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
3.6field-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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
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  11. Effect of Pituitary-Target Gland Axis on RAAS in the Context of COVID-19.International journal of medical sciences · 2025
    Review
  12. The glucocorticoid receptor potentiates aldosterone-induced transcription by the mineralocorticoid receptor.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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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

3 authors at 2 institutions in 1 country.

Robert W HunterUniversity/BHF Centre for Cardiovascular Science, The Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK. matthew.bailey@ed.ac.uk.
Jessica R Ivy
Matthew A Bailey
British Heart Foundation · GBUniversity of Edinburgh · GB

Funding

British Heart FoundationWellcome Trust
6 · The paper itself

Abstract

The clinical manifestations of glucocorticoid excess include central obesity, hyperglycaemia, dyslipidaemia, electrolyte abnormalities and hypertension. A century on from Cushing's original case study, these cardinal features are prevalent in industrialized nations. Hypertension is the major modifiable risk factor for cardiovascular and renal disease and reflects underlying abnormalities of Na(+) homeostasis. Aldosterone is a master regulator of renal Na(+) transport but here we argue that glucocorticoids are also influential, particularly during moderate excess. The hypothalamic-pituitary-adrenal axis can affect renal Na(+) homeostasis on multiple levels, systemically by increasing mineralocorticoid synthesis and locally by actions on both the mineralocorticoid and glucocorticoid receptors, both of which are expressed in the kidney. The kidney also expresses both of the 11β-hydroxysteroid dehydrogenase (11βHSD) enzymes. The intrarenal generation of active glucocorticoid by 11βHSD1 stimulates Na(+) reabsorption; failure to downregulate the enzyme during adaption to high dietary salt causes salt-sensitive hypertension. The deactivation of glucocorticoid by 11βHSD2 underpins the regulatory dominance for Na(+) transport of mineralocorticoids and defines the 'aldosterone-sensitive distal nephron'. In summary, glucocorticoids can stimulate renal transport processes conventionally attributed to the renin-angiotensin-aldosterone system. Importantly, Na(+) and volume homeostasis do not exert negative feedback on the hypothalamic-pituitary-adrenal axis. These actions are therefore clinically relevant and may contribute to the pathogenesis of hypertension in conditions associated with elevated glucocorticoid levels, such as the metabolic syndrome and chronic stress.

Indexed as

AnimalsGlucocorticoidsHumansHypertensionIon TransportKidneyRenin-Angiotensin SystemSodiumWater-Electrolyte BalanceGlucocorticoidsSodium

Identifiers

PMID24535442
PMCPMC4001748
OpenAlexW2098122042

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.