Evidence map›Paper›PMID 27141055›Full record

ArticleHypertension (Dallas, Tex. : 1979)2016

Impact of Angiotensin Type 1A Receptors in Principal Cells of the Collecting Duct on Blood Pressure and Hypertension.

Daian Chen, Johannes Stegbauer, Matthew A Sparks, Donald Kohan, Robert Griffiths, Marcela Herrera, Susan B Gurley, Thomas M Coffman

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.0field-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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Angiotensin II-Type-1a Receptor and Renal K + Wasting during Overnight Low-Na + Intake.Journal of the American Society of Nephrology : JASN · 2024
    Article
  3. Aldosterone-independent regulation of K + secretion in the distal nephron.Current opinion in nephrology and hypertension · 2024
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Landscape of GPCR expression along the mouse nephron.American journal of physiology. Renal physiology · 2021
    Article
  10. Vascular control of kidney epithelial transporters.American journal of physiology. Renal physiology · 2021
    Article
  11. Review
  12. Journal of the American Society of Nephrology : JASN · 2020
    Article
  13. Article
  14. Article
  15. Review
  16. PGELaboratory investigation; a journal of technical methods and pathology · 2018
    Article
  17. Review
  18. Article
  19. Review
  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

8 authors at 1 institution in 1 country.

Daian ChenFrom the Division of Nephrology, Department of Medicine, Duke University, and Durham VA Medical Centers, NC (D.C., M.A.S., R.G., M.H., S.B.G., T.M.C.); Department of Nephrology, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany (J.S.); School of Medicine, University of Utah Health Sciences Center, Salt Lake City (D.K.); and Cardiovascular and Metabolic Disorders Research Program, Duke-NUS Graduate Medical School, Singapore, Singapore (T.M.C.).
Johannes StegbauerFrom the Division of Nephrology, Department of Medicine, Duke University, and Durham VA Medical Centers, NC (D.C., M.A.S., R.G., M.H., S.B.G., T.M.C.); Department of Nephrology, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany (J.S.); School of Medicine, University of Utah Health Sciences Center, Salt Lake City (D.K.); and Cardiovascular and Metabolic Disorders Research Program, Duke-NUS Graduate Medical School, Singapore, Singapore (T.M.C.).
Matthew A SparksFrom the Division of Nephrology, Department of Medicine, Duke University, and Durham VA Medical Centers, NC (D.C., M.A.S., R.G., M.H., S.B.G., T.M.C.); Department of Nephrology, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany (J.S.); School of Medicine, University of Utah Health Sciences Center, Salt Lake City (D.K.); and Cardiovascular and Metabolic Disorders Research Program, Duke-NUS Graduate Medical School, Singapore, Singapore (T.M.C.).
Donald KohanFrom the Division of Nephrology, Department of Medicine, Duke University, and Durham VA Medical Centers, NC (D.C., M.A.S., R.G., M.H., S.B.G., T.M.C.); Department of Nephrology, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany (J.S.); School of Medicine, University of Utah Health Sciences Center, Salt Lake City (D.K.); and Cardiovascular and Metabolic Disorders Research Program, Duke-NUS Graduate Medical School, Singapore, Singapore (T.M.C.).
Robert GriffithsFrom the Division of Nephrology, Department of Medicine, Duke University, and Durham VA Medical Centers, NC (D.C., M.A.S., R.G., M.H., S.B.G., T.M.C.); Department of Nephrology, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany (J.S.); School of Medicine, University of Utah Health Sciences Center, Salt Lake City (D.K.); and Cardiovascular and Metabolic Disorders Research Program, Duke-NUS Graduate Medical School, Singapore, Singapore (T.M.C.).
Marcela HerreraFrom the Division of Nephrology, Department of Medicine, Duke University, and Durham VA Medical Centers, NC (D.C., M.A.S., R.G., M.H., S.B.G., T.M.C.); Department of Nephrology, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany (J.S.); School of Medicine, University of Utah Health Sciences Center, Salt Lake City (D.K.); and Cardiovascular and Metabolic Disorders Research Program, Duke-NUS Graduate Medical School, Singapore, Singapore (T.M.C.).
Susan B GurleyFrom the Division of Nephrology, Department of Medicine, Duke University, and Durham VA Medical Centers, NC (D.C., M.A.S., R.G., M.H., S.B.G., T.M.C.); Department of Nephrology, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany (J.S.); School of Medicine, University of Utah Health Sciences Center, Salt Lake City (D.K.); and Cardiovascular and Metabolic Disorders Research Program, Duke-NUS Graduate Medical School, Singapore, Singapore (T.M.C.).
Thomas M CoffmanFrom the Division of Nephrology, Department of Medicine, Duke University, and Durham VA Medical Centers, NC (D.C., M.A.S., R.G., M.H., S.B.G., T.M.C.); Department of Nephrology, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany (J.S.); School of Medicine, University of Utah Health Sciences Center, Salt Lake City (D.K.); and Cardiovascular and Metabolic Disorders Research Program, Duke-NUS Graduate Medical School, Singapore, Singapore (T.M.C.). tcoffman@duke.edu.
University of Utah · US

Funding

Renal Genomics CoreP30DK096493 · NIDDK · DUKE UNIVERSITY · PI FOSTER, MARY H., SVETKEY, LAURA P · 2012 to 2016
$5.9M
ANGIOTENSIN RECEPTOR GENES AND BLOOD PRESSURE REGULATIONR01HL056122 · NHLBI · DUKE UNIVERSITY · PI COFFMAN, THOMAS M · 1997 to 2010
$3.2M
Paracrine Control of Blood Pressure by Renal Intercalated CellsR01DK105049 · NIDDK · DUKE UNIVERSITY · PI COFFMAN, THOMAS M · 2015 to 2019
$1.8M
AT1 Angiotensin Receptors in the Renal Circulation Control Blood PressureIK2BX002240 · VA · DURHAM VA MEDICAL CENTER · PI SPARKS, MATTHEW AARON · 2014 to 2018
–
BLRD VA IK2 BX002240NHLBI NIH HHS R01 HL056122NIDDK NIH HHS P30 DK096493NIDDK NIH HHS R01 DK105049
6 · The paper itself

Abstract

The main actions of the renin-angiotensin system to control blood pressure (BP) are mediated by the angiotensin type 1 receptors (AT1Rs). The major murine AT1R isoform, AT1AR, is expressed throughout the nephron, including the collecting duct in both principal and intercalated cells. Principal cells play the major role in sodium and water reabsorption. Although aldosterone is considered to be the dominant regulator of sodium reabsorption by principal cells, recent studies suggest a role for direct actions of AT1R. To specifically examine the contributions of AT1AR in principal cells to BP regulation and the development of hypertension in vivo, we generated inbred 129/SvEv mice with deletion of AT1AR from principal cells (PCKO). At baseline, we found that BPs measured by radiotelemetry were similar between PCKOs and controls. During 1-week of low-salt diet (<0.02% NaCl), BPs fell significantly (P<0.05) and to a similar extent in both groups. On a high-salt (6% NaCl) diet, BP increased but was not different between groups. During the initial phase of angiotensin II-dependent hypertension, there was a modest but significant attenuation of hypertension in PCKOs (163±6 mm Hg) compared with controls (178±2 mm Hg; P<0.05) that was associated with enhanced natriuresis and decreased alpha epithelial sodium channel activation in the medulla of PCKOs. However, from day 9 onward, BPs were indistinguishable between groups. Although effects of AT1AR on baseline BP and adaptation to changes in dietary salt are negligible, our studies suggest that direct actions of AT1AR contribute to the initiation of hypertension and epithelial sodium channel activation.

Indexed as

Analysis of VarianceAngiotensin IIAnimalsBlood PressureCells, CulturedDisease Models, AnimalHypertensionKidney Tubules, CollectingMiceRandom AllocationReceptor, Angiotensin, Type 1Reference ValuesRenin-Angiotensin SystemAngiotensin IIReceptor, Angiotensin, Type 1angiotensin AT1A receptorangiotensin IIblood pressureepithelial sodium channel blockershypertension

Identifiers

PMID27141055
PMCPMC4865430
OpenAlexW2346864565

What OpenQuestion holds

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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.