Evidence map›Paper›PMID 24694992›Full record

ArticleKidney international2014

Deletion of the angiotensin II type 1 receptor-associated protein enhances renal sodium reabsorption and exacerbates angiotensin II-mediated hypertension.

Masato Ohsawa, Kouichi Tamura, Hiromichi Wakui, Akinobu Maeda, Toru Dejima, Tomohiko Kanaoka, Kengo Azushima, Kazushi Uneda, Yuko Tsurumi-Ikeya, Ryu Kobayashi and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Plants (Basel, Switzerland) · 2026
    Article
  3. The skin renin-angiotensin system and hypertension: A TRAP for blood flow capture and water release.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. ATRAP, a receptor-interacting modulator of kidney physiology, as a novel player in blood pressure and beyond.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Aristolochic Acid Induces Renal Fibrosis and Senescence in Mice.International journal of molecular sciences · 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

18 authors at 3 institutions in 1 country.

Masato OhsawaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Kouichi TamuraDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Hiromichi WakuiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Akinobu MaedaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Toru DejimaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Tomohiko KanaokaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Kengo AzushimaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Kazushi UnedaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Yuko Tsurumi-IkeyaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Ryu KobayashiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Miyuki MatsudaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Shinichi UchidaDepartment of Nephrology, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Yoshiyuki ToyaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Hiroyuki KoboriDepartment of Pharmacology, Kagawa University School of Medicine, Kagawa, Japan.
Akira NishiyamaDepartment of Pharmacology, Kagawa University School of Medicine, Kagawa, Japan.
Akio YamashitaDepartment of Molecular Biology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Yoshihiro IshikawaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Satoshi UmemuraDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Yokohama City University · JPKagawa University · JPTokyo Medical and Dental University · JP

Funding

Intrarenal Augmentation of Angiotensinogen by Ang IIR01DK072408 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI NAVAR, LUIS GABRIEL · 2006 to 2010
$1.2M
NIDDK NIH HHS R01 DK072408
6 · The paper itself

Abstract

Angiotensin II type 1 receptor (AT1R)-associated protein (ATRAP) promotes AT1R internalization along with suppression of pathological activation of tissue AT1R signaling. However, the functional significance of ATRAP in renal sodium handling and blood pressure regulation under pathological stimuli is not fully resolved. Here we show the blood pressure of mice with a gene-targeted disruption of ATRAP was comparable to that of wild-type mice at baseline. However, in ATRAP-knockout mice, angiotensin II-induced hypertension was exacerbated and the extent of positive sodium balance was increased by angiotensin II. Renal expression of the sodium-proton antiporter 3, a major sodium transporter in the proximal tubules, urinary pH, renal angiotensinogen production, and angiotensin II content was unaffected. Stimulation of the renal expression and activity of the epithelial sodium channel (ENaC), a major sodium transporter in the distal tubules, was significantly enhanced by chronic angiotensin II infusion. The circulating and urinary aldosterone levels were comparable. The blood pressure response and renal ENaC expression by aldosterone were not affected. Thus, ATRAP deficiency exacerbated angiotensin II-mediated hypertension by pathological activation of renal tubular AT1R by angiotensin II. This directly stimulates ENaC in the distal tubules and enhances sodium retention in an aldosterone-independent manner.

Indexed as

Adaptor Proteins, Signal TransducingAldosteroneAngiotensin IIAngiotensinogenAnimalsBlood PressureEpithelial Sodium ChannelsGene DeletionHydrogen-Ion ConcentrationHypertensionKidney Tubules, DistalKidney Tubules, ProximalMaleMiceMice, Inbred C57BLMice, KnockoutAdaptor Proteins, Signal TransducingAgtrap protein, mouseAldosteroneAngiotensin IIAngiotensinogenEpithelial Sodium ChannelsReceptor, Angiotensin, Type 1RNA, MessengerSodiumSodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersVasoconstrictor Agents

Identifiers

PMID24694992
PMCPMC4149871
OpenAlexW1965175129

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.