Evidence map›Paper›PMID 26554902›Full record

ArticleBMC medicine2015

Renal medullary (pro)renin receptor contributes to angiotensin II-induced hypertension in rats via activation of the local renin-angiotensin system.

Fei Wang, Xiaohan Lu, Mi Liu, Yumei Feng, Shu-Feng Zhou, Tianxin Yang

Open access · goldAbstract read
In one paragraph

Article in BMC medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 77 citations in OpenAlex.

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  14. Role of (pro)renin receptor in cyclosporin A-induced nephropathy.American journal of physiology. Renal physiology · 2022
    Article
  15. Article
  16. Soluble (Pro)Renin Receptor as a Negative Regulator of NCC (NaHypertension (Dallas, Tex. : 1979) · 2021
    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

6 authors at 4 institutions in 2 countries.

Fei WangInstitute of Hypertension, Sun Yat-sen University School of Medicine, #74 Zhongshan 2nd Road, Science and Technology Building, 6th Floor, Guangzhou, 510080, P. R. China.
Xiaohan LuInstitute of Hypertension, Sun Yat-sen University School of Medicine, #74 Zhongshan 2nd Road, Science and Technology Building, 6th Floor, Guangzhou, 510080, P. R. China.
Mi LiuInstitute of Hypertension, Sun Yat-sen University School of Medicine, #74 Zhongshan 2nd Road, Science and Technology Building, 6th Floor, Guangzhou, 510080, P. R. China.
Yumei FengDepartments of Pharmacology and Physiology & Cell Biology, University of Nevada School of Medicine, Reno, NE, USA.
Shu-Feng ZhouDepartment of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL, USA.
Tianxin YangInstitute of Hypertension, Sun Yat-sen University School of Medicine, #74 Zhongshan 2nd Road, Science and Technology Building, 6th Floor, Guangzhou, 510080, P. R. China. Yangtxin@mail.sysu.edu.cn.
Sun Yat-sen University · CNUniversity of Utah · USUniversity of Nevada, Reno · USUniversity of South Florida · US

Funding

The Neural Mechanisms of HypertensionR01HL122770 · NHLBI · UNIVERSITY OF ROCHESTER · PI EARLEY, SCOTT, FENG EARLEY, YUMEI · 2015 to 2023
$4.2M
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
NHLBI NIH HHS R01 HL122770NIDDK NIH HHS DK094956NIDDK NIH HHS DK104072NIDDK NIH HHS R01 DK094956NIDDK NIH HHS R01 DK104072
6 · The paper itself

Abstract

background(Pro)renin receptor (PRR) is a new component of the renin-angiotensin system and regulates renin activity in vitro. Within the kidney, PRR is highly expressed in the renal medulla where its expression is induced by angiotensin II infusion. The objective of the present study was to test a potential role of renal medullary PRR during angiotensin II-induced hypertension.

methodsA rat AngII infusion model (100 ng/kg/min) combined with renal intramedullary infusion of PRO20, a specific inhibitor of PRR, was builded. And the intravenous PRO20 infusion serve as control. Mean arterial pressure was recorded by radiotelemetry for one week. Further analysis of kidney injury, inflammation, biochemical indices and protein localization were performed in vivo or in vitro.

resultsRadiotelemetry demonstrated that AngII infusion elevated the mean arteria pressure from 108 ± 5.8 to 164.7 ± 6.2 mmHg. Mean arterial pressure decreased to 128.6 ± 5.8 mmHg (P < 0.05) after intramedullary infusion of PRO20, but was only modestly affected by intravenous PRO20 infusion. Indices of kidney injury, including proteinuria, glomerulosclerosis, and interstitial fibrosis, inflammation, and increased renal medullary and urinary renin activity following angiotensin II infusion were all remarkably attenuated by intramedullary PRO20 infusion. Following one week of angiotensin II infusion, increased PRR immunoreactivity was found in vascular smooth muscle cells. In cultured rat vascular smooth muscle cells, angiotensin II induced parallel increases in soluble PRR and renin activity, and the latter was significantly reduced by PRO20.

conclusionRenal medullary PRR mediates angiotensin II-induced hypertension, likely by amplifying the local renin response.

Indexed as

Angiotensin IIAnimalsHypertensionMaleMuscle, Smooth, VascularRatsReceptors, Cell SurfaceReninRenin-Angiotensin SystemAngiotensin IIReceptors, Cell SurfaceRenin

Identifiers

PMID26554902
PMCPMC4641338
OpenAlexW2189396410

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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.