Evidence map›Paper›PMID 27993957›Full record

ArticleHypertension (Dallas, Tex. : 1979)2017

Activation of Renal (Pro)Renin Receptor Contributes to High Fructose-Induced Salt Sensitivity.

Chuanming Xu, Aihua Lu, Xiaohan Lu, Linlin Zhang, Hui Fang, Li Zhou, Tianxin Yang

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
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  6. ProbioticsmSystems · 2023
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  19. Soluble (Pro)Renin Receptor as a Negative Regulator of NCC (NaHypertension (Dallas, Tex. : 1979) · 2021
    Article
  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

7 authors at 1 institution in 1 country.

Chuanming XuFrom the Institute of Hypertension, Sun Yat-Sen University School of Medicine, Guangzhou, China (C.X., A.L., X.L., L.Z., H.F., L.Z., T.Y.); Internal Medicine, University of Utah, Salt Lake City (C.X., X.L., T.Y.); and Veterans Affairs Medical Center, Salt Lake City, Utah (X.L., T.Y.).
Aihua LuFrom the Institute of Hypertension, Sun Yat-Sen University School of Medicine, Guangzhou, China (C.X., A.L., X.L., L.Z., H.F., L.Z., T.Y.); Internal Medicine, University of Utah, Salt Lake City (C.X., X.L., T.Y.); and Veterans Affairs Medical Center, Salt Lake City, Utah (X.L., T.Y.).
Xiaohan LuFrom the Institute of Hypertension, Sun Yat-Sen University School of Medicine, Guangzhou, China (C.X., A.L., X.L., L.Z., H.F., L.Z., T.Y.); Internal Medicine, University of Utah, Salt Lake City (C.X., X.L., T.Y.); and Veterans Affairs Medical Center, Salt Lake City, Utah (X.L., T.Y.).
Linlin ZhangFrom the Institute of Hypertension, Sun Yat-Sen University School of Medicine, Guangzhou, China (C.X., A.L., X.L., L.Z., H.F., L.Z., T.Y.); Internal Medicine, University of Utah, Salt Lake City (C.X., X.L., T.Y.); and Veterans Affairs Medical Center, Salt Lake City, Utah (X.L., T.Y.).
Hui FangFrom the Institute of Hypertension, Sun Yat-Sen University School of Medicine, Guangzhou, China (C.X., A.L., X.L., L.Z., H.F., L.Z., T.Y.); Internal Medicine, University of Utah, Salt Lake City (C.X., X.L., T.Y.); and Veterans Affairs Medical Center, Salt Lake City, Utah (X.L., T.Y.).
Li ZhouFrom the Institute of Hypertension, Sun Yat-Sen University School of Medicine, Guangzhou, China (C.X., A.L., X.L., L.Z., H.F., L.Z., T.Y.); Internal Medicine, University of Utah, Salt Lake City (C.X., X.L., T.Y.); and Veterans Affairs Medical Center, Salt Lake City, Utah (X.L., T.Y.).
Tianxin YangFrom the Institute of Hypertension, Sun Yat-Sen University School of Medicine, Guangzhou, China (C.X., A.L., X.L., L.Z., H.F., L.Z., T.Y.); Internal Medicine, University of Utah, Salt Lake City (C.X., X.L., T.Y.); and Veterans Affairs Medical Center, Salt Lake City, Utah (X.L., T.Y.). Tianxin.Yang@hsc.utah.edu.
University of Utah · US

Funding

Interaction of PGE2 and intrarenal RAS in AngII-induced hypertensionR01DK104072 · NIDDK · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI YANG, TIANXIN · 2015 to 2025
$3.7M
Control of collecting duct function by lipid-derived factors in obesityR01DK094956 · NIDDK · UNIVERSITY OF UTAH · PI YANG, TIANXIN · 2013 to 2017
$1.6M
Role of renal (pro)renin receptor in hypertension and kidney injuryI01BX002817 · VA · VA SALT LAKE CITY HEALTHCARE SYSTEM · PI YANG, TIANXIN · 2017 to 2020
–
BLRD VA I01 BX002817NIDDK NIH HHS R01 DK094956NIDDK NIH HHS R01 DK104072
6 · The paper itself

Abstract

A high-fructose diet is shown to induce salt-sensitive hypertension, but the underlying mechanism largely remains unknown. The major goal of the present study was to test the role of renal (pro)renin receptor (PRR) in this model. In Sprague-Dawley rats, high-fructose intake increased renal expression of full-length PRR, which were attenuated by allopurinol. High-fructose intake also upregulated renal mRNA and protein expression of sodium/hydrogen exchanger 3 and Na/K/2Cl cotransporter, as well as in vivo Na/K/2Cl cotransporter activity, all of which were nearly completely blocked by a PRR decoy inhibitor PRO20 or allopurinol treatment. Parallel changes were observed for indices of intrarenal renin-angiotensin-system including renal and urinary renin and angiotensin II levels. Radiotelemetry demonstrated that high-fructose or a high-salt diet alone did not affect mean arterial pressure, but the combination of the 2 maneuvers induced a ≈10-mm Hg increase of mean arterial pressure, which was blunted by PRO20 or allopurinol treatment. In cultured human kidney 2 cells, both fructose and uric acid increased protein expression of soluble PRR in a time- and dose-dependent manner; fructose-induced PRR upregulation was inhibited by allopurinol. Taken together, our data suggest that fructose via uric acid stimulates renal expression of PRR/soluble PRR that stimulate sodium/hydrogen exchanger 3 and Na/K/2Cl cotransporter expression and intrarenal renin-angiotensin system to induce salt-sensitive hypertension.

Indexed as

AllopurinolAnimalsCells, CulturedDisease Models, AnimalFructoseHumansHypertensionKidneyMaleProrenin ReceptorRatsRats, Sprague-DawleyReceptors, Cell SurfaceRenin-Angiotensin SystemAllopurinolFructoseProrenin ReceptorReceptors, Cell Surfacefructose diethypertensionrenin–angiotensin systemuric acid

Identifiers

PMID27993957
PMCPMC5556690
OpenAlexW2565680418

What OpenQuestion holds

Textmetadata
LicenceTDM
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.