Evidence map›Paper›PMID 31097611›Full record

ArticleJournal of the American Society of Nephrology : JASN2019

Vasopressin Increases Urinary Acidification

Torsten Giesecke, Nina Himmerkus, Jens Leipziger, Markus Bleich, Taka-Aki Koshimizu, Michael Fähling, Alina Smorodchenko, Julia Shpak, Carolin Knappe, Julian Isermann and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Novel Roles of GPCRs in the Renal Collecting Duct.Physiology (Bethesda, Md.) · 2026
    Review
  2. Article
  3. Article
  4. GDF15, an Emerging Player in Renal Physiology and Pathophysiology.International journal of molecular sciences · 2024
    Review
  5. Secretin: a hormone for HCOPflugers Archiv : European journal of physiology · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Urinary Lithogenic Risk Profile in ADPKD Patients Treated with Tolvaptan.Clinical journal of the American Society of Nephrology : CJASN · 2020
    Article
  17. 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

17 authors at 7 institutions in 4 countries.

Torsten GieseckeInstitute of Vegetative Anatomy, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany; kerim.mutig@charite.de torsten.giesecke@charite.de.ORCID 0000-0002-6658-5027
Nina HimmerkusInstitute of Physiology, Christian-Albrechts-Universität zu Kiel, Kiel, Germany.
Jens LeipzigerDepartment of Biomedicine, Aarhus University, Aarhus C, Denmark.
Markus BleichInstitute of Physiology, Christian-Albrechts-Universität zu Kiel, Kiel, Germany.
Taka-Aki KoshimizuDivision of Molecular Pharmacology, Department of Pharmacology, Jichi Medical University, Shimotsuke-shi, Tochigi-ken, Japan.
Michael FählingInstitute of Vegetative Physiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Alina SmorodchenkoInstitute of Vegetative Anatomy, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Julia ShpakInstitute of Vegetative Anatomy, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Carolin KnappeInstitute of Vegetative Anatomy, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Julian IsermannInstitute of Physiology, Christian-Albrechts-Universität zu Kiel, Kiel, Germany.
Niklas AyasseDepartment of Biomedicine, Aarhus University, Aarhus C, Denmark.
Katsumasa KawaharaDepartment of Physiology, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.
Jan SchmoranzerAdvanced Medical BioImaging Core Facility, Charite-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Niclas GimberAdvanced Medical BioImaging Core Facility, Charite-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Alexander PaliegeDivision of Nephrology, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Dresden, Germany; and.
Sebastian BachmannInstitute of Vegetative Anatomy, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Kerim MutigInstitute of Vegetative Anatomy, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany; kerim.mutig@charite.de torsten.giesecke@charite.de.
Humboldt-Universität zu Berlin · DEChristian-Albrechts-Universität zu Kiel · DEAarhus University · DKJichi Medical University · JPKitasato University · JPSechenov University · RUUniversity Hospital Carl Gustav Carus · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAntagonists of the V1a vasopressin receptor (V1aR) are emerging as a strategy for slowing progression of CKD. Physiologically, V1aR signaling has been linked with acid-base homeostasis, but more detailed information is needed about renal V1aR distribution and function.

methodsWe used a new anti-V1aR antibody and high-resolution microscopy to investigate Va1R distribution in rodent and human kidneys. To investigate whether V1aR activation promotes urinary H

resultsLocalization of V1aR in rodent and human kidneys produced a basolateral signal in type A intercalated cells (A-ICs) and a perinuclear to subapical signal in type B intercalated cells of connecting tubules and collecting ducts. Treating vasopressin-deficient Brattleboro rats with a V1aR agonist decreased urinary pH and tripled net acid excretion; we observed a similar response in C57BL/6J mice. In contrast, V1aR antagonist did not affect urinary pH in normal or acid-loaded mice. In

conclusionsOur results show that activation of V1aR contributes to urinary acidification

Indexed as

Acid-Base EquilibriumAnimalsCells, CulturedEpithelial CellsFluorescent Antibody TechniqueHEK293 CellsHumansHydrogen-Ion ConcentrationImmunohistochemistryKidney Tubules, CollectingMaleMice, Inbred C57BLRats, BrattleboroRats, WistarReal-Time Polymerase Chain ReactionReceptors, VasopressinAVPR1A protein, humanReceptors, VasopressinVasopressinsacid-base homeostasisantidiuretic hormonedistal renal tubular acidosisintercalated cellsvasopressin V1a receptorV-ATPase

Identifiers

PMID31097611
PMCPMC6551786
OpenAlexW2946497163

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.