Evidence map›Paper›PMID 26755736›Full record

ArticlePhysiological reports2016

Possible role for nephron-derived angiotensinogen in angiotensin-II dependent hypertension.

Nirupama Ramkumar, Deborah Stuart, Matias Calquin, Shuping Wang, Fumio Niimura, Taiji Matsusaka, Donald E Kohan

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 13% 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, 19 citations in OpenAlex.

  1. Article
  2. The relationship between estrogen and renin angiotensin system components in the context of hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
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  12. Physiology and Pathophysiology of the Intrarenal Renin-Angiotensin System: An Update.Journal of the American Society of Nephrology : JASN · 2017
    Review
  13. Review
  14. 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

7 authors at 3 institutions in 2 countries.

Nirupama RamkumarDivision of Nephrology and Hypertension, University of Utah Health Sciences Center, Salt Lake City, Utah nirupama.ramkumar@hsc.utah.edu.
Deborah StuartDivision of Nephrology and Hypertension, University of Utah Health Sciences Center, Salt Lake City, Utah.
Matias CalquinDivision of Nephrology and Hypertension, University of Utah Health Sciences Center, Salt Lake City, Utah.
Shuping WangDivision of Nephrology and Hypertension, University of Utah Health Sciences Center, Salt Lake City, Utah.
Fumio NiimuraInstitute of Medical Science, Tokai University, Isehara, Japan.
Taiji MatsusakaInstitute of Medical Science, Tokai University, Isehara, Japan.
Donald E KohanDivision of Nephrology and Hypertension, University of Utah Health Sciences Center, Salt Lake City, Utah Veterans Affairs Medical Center, Salt Lake City, Utah.
University of Utah · USTokai University · JPUniversity of Utah Health Care · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of intranephron angiotensinogen (AGT) in blood pressure (BP) regulation is not fully understood. Previous studies showed that proximal tubule-specific overexpression of AGT increases BP, whereas proximal tubule-specific deletion of AGT did not alter BP. The latter study may not have completely eliminated nephron AGT production; in addition, BP was only assessed on a normal salt diet. To evaluate this issue in greater detail, we developed mice with inducible nephron-wide AGT deletion. Mice were generated which were hemizygous for the Pax8-rtTA and LC-1 transgenes and homozygous for loxP-flanked AGT alleles to achieve nephron-wide AGT disruption after doxycycline induction. Compared to controls, AGT knockout (KO) mice demonstrated markedly reduced renal AGT immunostaining, mRNA, and protein levels; unexpectedly AGT KO mice had reduced AGT mRNA levels in the liver along with 50% reduction in plasma AGT levels. BP was significantly lower in the AGT KO mice compared to controls fed a normal, low, or high Na(+) intake, with the highest BP reduction on a low Na(+) diet. Regardless of Na(+) intake, AGT KO mice had higher plasma renin concentration (PRC) and markedly reduced urinary AGT levels compared to controls. Following angiotensin-II (Ang-II) infusion, AGT KO mice demonstrated an attenuated hypertensive response despite similar suppression of PRC in the two groups. Taken together, these data suggest that nephron-derived AGT may be involved in Ang-II-dependent hypertension, however, a clear role for nephron-derived AGT in physiological BP regulation remains to be determined.

Indexed as

Angiotensin IIAngiotensinogenAnimalsHypertensionMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNephronsSodium, DietaryAngiotensin IIAngiotensinogenSodium, DietaryAngiotensinogenblood pressurekidneyliver

Identifiers

PMID26755736
PMCPMC4760401
OpenAlexW2276443850

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.