Evidence map›Paper›PMID 19387470›Full record

ArticleKidney international2009

AT1a receptor knockout in mice impairs urine concentration by reducing basal vasopressin levels and its receptor signaling proteins in the inner medulla.

Xiao C Li, Yuan Shao, Jia L Zhuo

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.7field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Genetic Deletion of ATInternational journal of molecular sciences · 2022
    Article
  3. Angiotensin II and ATInternational journal of molecular sciences · 2022
    Review
  4. Article
  5. The NaFrontiers in physiology · 2022
    Review
  6. Targeting the Trafficking of Kidney Water Channels for Therapeutic Benefit.Annual review of pharmacology and toxicology · 2020
    Review
  7. Soluble (pro)renin receptor as a potential therapy for diabetes insipidus.American journal of physiology. Renal physiology · 2018
    Review
  8. Review
  9. Article
  10. Review
  11. PGELaboratory investigation; a journal of technical methods and pathology · 2018
    Article
  12. Article
  13. Article
  14. Vasopressin/V2 receptor stimulates renin synthesis in the collecting duct.American journal of physiology. Renal physiology · 2016
    Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. ANG II receptor subtype 1a gene knockdown in the subfornical organ prevents increased drinking behavior in bile duct-ligated rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2014
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Xiao C LiLaboratory of Receptor and Signal Transduction, Division of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan 48202, USA.
Yuan Shao
Jia L Zhuo
Henry Ford Hospital · USWayne State University · US

Funding

Role of Intracrine Angiotensin II in Kidney CellsR01DK067299 · NIDDK · UNIVERSITY OF MISSISSIPPI MED CTR · PI Jia Long Zhuo · 2004 to 2026
$6.5M
Novel Roles of Intracrine Angiotensin II in Proximal Tubule CellsR56DK067299 · NIDDK · HENRY FORD HEALTH SYSTEM · PI ZHUO, JIA LONG · 2009 to 2009
$352k
NIDDK NIH HHS 5R01DK067299NIDDK NIH HHS R01 DK067299NIDDK NIH HHS R56 DK067299
6 · The paper itself

Abstract

Angiotensin II plays an important role in the regulation of blood pressure, body salt and fluid balance, and urine concentration. Mice with deletion of the AT(1a) receptor develop polyuria and urine concentration defects. We studied the mechanisms of these urine concentration defects by treating wild-type and AT(1a)-knockout mice with arginine vasopressin (AVP) for 2 weeks, controlling their water intake, or giving them an osmotic diuretic (sucrose) in order to determine whether central or nephrogenic mechanisms were involved. Under basal conditions, AT(1a)-knockout mice were hypotensive, had lower plasma AVP, and excreted more urine with a markedly reduced osmolality compared with wild-type mice. However, basal glomerular filtration rates were similar in both strains of mice. We isolated total lysate and membrane proteins from the inner medulla of wild-type and mutant mouse kidneys, and found that the amounts of aquaporin 2 (AQP2), adenylyl cyclases III and V/VI, and phosphorylated MAP kinases ERK 1/2 proteins were all reduced in the inner medulla of the knockout mice. Infusion of AVP raised plasma levels and blood pressure proportionally in both strains, but polyuria persisted and urine osmolality remained significantly lower in the knockout mice. Although AVP increased urine osmolality slightly in water-deprived knockout mice, this was well below the basal osmolality of wild-type mice. The diuretic response to the hyperosmotic sucrose was also impaired in the knockout mice. Neither AVP nor water rationing restored the levels of the inner medullary signaling proteins and membrane AQP2 proteins in the knockout mice. We suggest that AT(1a) receptor deletion causes polyuria and urine concentration defects by decreasing basal AVP release and impairing AVP-induced receptor signaling in the inner medulla.

Indexed as

Kidney Concentrating AbilityAnimalsAntidiuretic AgentsAquaporin 2Arginine VasopressinHypotensionKidney MedullaMiceMice, KnockoutPolyuriaReceptor, Angiotensin, Type 1Receptors, VasopressinVasopressinsAntidiuretic AgentsAqp2 protein, mouseAquaporin 2Arginine VasopressinReceptor, Angiotensin, Type 1Receptors, VasopressinVasopressins

Identifiers

PMID19387470
PMCPMC2760268
OpenAlexW2004250198

What OpenQuestion holds

Textmetadata
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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.