Evidence map›Paper›PMID 15841186›Full record

ArticleThe Journal of clinical investigation2005

Distinct roles for the kidney and systemic tissues in blood pressure regulation by the renin-angiotensin system.

Steven D Crowley, Susan B Gurley, Michael I Oliverio, A Kathy Pazmino, Robert Griffiths, Patrick J Flannery, Robert F Spurney, Hyung-Suk Kim, Oliver Smithies, Thu H Le and 1 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed
12.5field-weighted citation impact, top 1% 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

180 citing papers in PubMed, 349 citations in OpenAlex.

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  6. 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
    Review
  7. Article
  8. A key role of ATAmerican journal of physiology. Renal physiology · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Hold the salt for kidney regeneration.The Journal of clinical investigation · 2024
    Article
  13. Review
  14. Histamine HPflugers Archiv : European journal of physiology · 2024
    Article
  15. Article
  16. Article
  17. Dopamine Receptor DThe Yale journal of biology and medicine · 2023
    Review
  18. Article
  19. Article
  20. Genetic Deletion of ATInternational journal of molecular sciences · 2022
    Article

120 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Steven D CrowleyDivision of Nephrology, Department of Medicine, Duke University and Durham VA Medical Centers, Durham, North Carolina 27705, USA.
Susan B Gurley
Michael I Oliverio
A Kathy Pazmino
Robert Griffiths
Patrick J Flannery
Robert F Spurney
Hyung-Suk Kim
Oliver Smithies
Thu H Le
Thomas M Coffman
Durham VA Medical Center · USDuke University · USUniversity of North Carolina at Chapel Hill · US

Funding

MODELS FOR STUDYING THE GENETICS OF HYPERTENSIONR01HL049277 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAEDA, NOBUYO · 1992 to 2025
$17.5M
ANGIOTENSIN RECEPTOR GENES AND BLOOD PRESSURE REGULATIONR01HL056122 · NHLBI · DUKE UNIVERSITY · PI COFFMAN, THOMAS M · 1997 to 2010
$3.2M
NHLBI NIH HHS HL49277NHLBI NIH HHS HL56122NHLBI NIH HHS R01 HL049277NHLBI NIH HHS R01 HL056122
6 · The paper itself

Abstract

Angiotensin II, acting through type 1 angiotensin (AT(1)) receptors, has potent effects that alter renal excretory mechanisms. Control of sodium excretion by the kidney has been suggested to be the critical mechanism for blood pressure regulation by the renin-angiotensin system (RAS). However, since AT(1) receptors are ubiquitously expressed, precisely dissecting their physiological actions in individual tissue compartments including the kidney with conventional pharmacological or gene targeting experiments has been difficult. Here, we used a cross-transplantation strategy and AT(1A) receptor-deficient mice to demonstrate distinct and virtually equivalent contributions of AT(1) receptor actions in the kidney and in extrarenal tissues to determining the level of blood pressure. We demonstrate that regulation of blood pressure by extrarenal AT(1A) receptors cannot be explained by altered aldosterone generation, which suggests that AT(1) receptor actions in systemic tissues such as the vascular and/or the central nervous systems make nonredundant contributions to blood pressure regulation. We also show that interruption of the AT(1) receptor-mediated short-loop feedback in the kidney is not sufficient to explain the marked stimulation of renin production induced by global AT(1) receptor deficiency or by receptor blockade. Instead, the renin response seems to be primarily determined by renal baroreceptor mechanisms triggered by reduced blood pressure. Thus, the regulation of blood pressure by the RAS is mediated by AT(1) receptors both within and outside the kidney.

Indexed as

Kidney TransplantationAdrenalectomyAldosteroneAngiotensin IIAnimalsBlood PressureBlood Pressure DeterminationDietHomeostasisKidneyMiceMice, Inbred C57BLMice, KnockoutNorepinephrineReceptor, Angiotensin, Type 1ReninAldosteroneAngiotensin IINorepinephrineReceptor, Angiotensin, Type 1ReninSalts

Identifiers

PMID15841186
PMCPMC1070417
OpenAlexW2157109450

What OpenQuestion holds

Textmetadata
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.