Evidence map›Paper›PMID 25792129›Full record

ArticleJournal of the American Heart Association2015

Renal tubule angiotensin II type 1 receptor-associated protein promotes natriuresis and inhibits salt-sensitive blood pressure elevation.

Hiromichi Wakui, Kazushi Uneda, Kouichi Tamura, Masato Ohsawa, Kengo Azushima, Ryu Kobayashi, Kohji Ohki, Toru Dejima, Tomohiko Kanaoka, Yuko Tsurumi-Ikeya and 7 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Effects of excess sodium consumption on arterial function in C57BL/6 mice.American journal of physiology. Heart and circulatory physiology · 2024
    Pooled it
  2. 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
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  7. 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
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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

17 authors at 2 institutions in 1 country.

Hiromichi WakuiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Kazushi UnedaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Kouichi TamuraDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Masato OhsawaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Kengo AzushimaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Ryu KobayashiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Kohji OhkiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Toru DejimaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Tomohiko KanaokaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Yuko Tsurumi-IkeyaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Miyuki MatsudaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Kotaro HaruharaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Akira NishiyamaDepartment of Pharmacology, Kagawa University School of Medicine, Kagawa, Japan (A.N.).
Machiko YabanaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Tetsuya FujikawaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Akio YamashitaDepartment of Molecular Biology, Yokohama City University Graduate School of Medicine, Yokohama, Japan (A.Y.).
Satoshi UmemuraDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan (H.W., K.U., K.T., M.O., K.A., R.K., K.O., T.D., T.K., Y.T.I., M.M., K.H., M.Y., T.F., S.U.).
Yokohama City University · JPKagawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAngiotensin II type 1 receptor (AT1R)-associated protein (ATRAP; Agtrap gene) promotes AT1R internalization along with suppression of pathological AT1R activation. In this study, we examined whether enhancement of ATRAP in the renal distal tubules affects sodium handling and blood pressure regulation in response to high salt (HS) loading, using ATRAP transgenic mice on a salt-sensitive C57BL/6J background. METHODS AND

resultsRenal ATRAP transgenic (rATRAP-Tg) mice, which exhibit renal tubule-dominant ATRAP enhancement, and their wild-type littermate C57BL/6J mice on a normal salt diet (0.3% NaCl) at baseline were subjected to dietary HS loading (4% NaCl) for 7 days. In rATRAP-Tg mice, the dietary HS loading-mediated blood pressure elevation was suppressed compared with wild-type mice, despite similar baseline blood pressure. Although renal angiotensin II level was comparable in rATRAP-Tg and wild-type mice with and without HS loading, urinary sodium excretion in response to HS loading was significantly enhanced in the rATRAP-Tg mice. In addition, functional transport activity of the amiloride-sensitive epithelial Na(+) channel was significantly decreased under saline volume-expanded conditions in rATRAP-Tg mice compared with wild-type mice, without any evident change in epithelial Na(+) channel protein expression. Plasma membrane AT1R expression in the kidney of rATRAP-Tg mice was decreased compared with wild-type mice.

conclusionsThese results demonstrated that distal tubule-dominant enhancement of ATRAP inhibits pathological renal sodium reabsorption and blood pressure elevation in response to HS loading. The findings suggest that ATRAP-mediated modulation of sodium handling in renal distal tubules could be a target of interest in salt-sensitive blood pressure regulation.

Indexed as

Blood PressureNatriuresisSodium Chloride, DietaryAdaptor Proteins, Signal TransducingAmilorideAngiotensin IIAnimalsBiomarkersCell MembraneDisease Models, AnimalEpithelial Sodium Channel BlockersEpithelial Sodium ChannelsHypertensionKidney Tubules, DistalMice, Inbred C57BLMice, TransgenicAdaptor Proteins, Signal TransducingAgtrap protein, mouseAmilorideAngiotensin IIBiomarkersEpithelial Sodium Channel BlockersEpithelial Sodium ChannelsReceptor, Angiotensin, Type 1Sodium Chloride, Dietaryangiotensin receptorsbasic sciencegene expression/regulationhypertension (kidney)receptorssalt‐sensitivesodium transport (kidney)

Identifiers

PMID25792129
PMCPMC4392439
OpenAlexW2156085358

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.