Evidence map›Paper›PMID 24431204›Full record

ArticleAmerican journal of physiology. Renal physiology2014

Lack of an effect of collecting duct-specific deletion of adenylyl cyclase 3 on renal Na+ and water excretion or arterial pressure.

Wararat Kittikulsuth, Deborah Stuart, Alfred N Van Hoek, James D Stockand, Vladislav Bugaj, Elena Mironova, Mitsi A Blount, Donald E Kohan

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2014. 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
1.4field-weighted citation impact, top 19% 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, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Adenylyl cyclase 3 regulates osteocyte mechanotransduction and primary cilium.Biochemical and biophysical research communications · 2021
    Article
  4. Stimulation of the Epithelial NaFrontiers in physiology · 2021
    Article
  5. Review
  6. Renal NaAmerican journal of physiology. Renal physiology · 2019
    Article
  7. Article
  8. Article
  9. Review
  10. Molecular mechanisms regulating aquaporin-2 in kidney collecting duct.American journal of physiology. Renal physiology · 2016
    Review
  11. Review
  12. Article
  13. Vasopressin/V2 receptor stimulates renin synthesis in the collecting duct.American journal of physiology. Renal physiology · 2016
    Article
  14. Article
  15. Article
  16. Regulation of nephron water and electrolyte transport by adenylyl cyclases.American journal of physiology. Renal physiology · 2014
    Review
  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

8 authors at 3 institutions in 1 country.

Wararat KittikulsuthDiv. of Nephrology, Univ. of Utah Health Sciences Center, 1900 East 30 North, Salt Lake City, UT 84132. donald.kohan@hsc.utah.edu.
Deborah Stuart
Alfred N Van Hoek
James D Stockand
Vladislav Bugaj
Elena Mironova
Mitsi A Blount
Donald E Kohan
University of Utah · USThe University of Texas Health Science Center at San Antonio · USEmory University · US

Funding

Role of adenylyl cyclase isoforms in collecting duct physiology & pathophysiologyR01DK097007 · NIDDK · UNIVERSITY OF UTAH · PI KOHAN, DONALD E · 2013 to 2016
$1.3M
NIDDK NIH HHS R01 DK097007NIDDK NIH HHS R01-DK-097007
6 · The paper itself

Abstract

cAMP is a key mediator of connecting tubule and collecting duct (CD) Na(+) and water reabsorption. Studies performed in vitro have suggested that CD adenylyl cyclase (AC)3 partly mediates the actions of vasopressin; however, the physiological role of CD AC3 has not been determined. To assess this, mice were developed with CD-specific disruption of AC3 [CD AC3 knockout (KO)]. Inner medullary CDs from these mice exhibited 100% target gene recombination and had reduced ANG II- but not vasopressin-induced cAMP accumulation. However, there were no differences in urine volume, urinary urea excretion, or urine osmolality between KO and control mice during normal water intake or varying degrees of water restriction in the presence or absence of chronic vasopressin administration. There were no differences between CD AC3 KO and control mice in arterial pressure or urinary Na(+) or K(+) excretion during a normal or high-salt diet, whereas plasma renin and vasopressin concentrations were similar between the two genotypes. Patch-clamp analysis of split-open cortical CDs revealed no difference in epithelial Na(+) channel activity in the presence or absence of vasopressin. Compensatory changes in AC6 were not responsible for the lack of a renal phenotype in CD AC3 KO mice since combined CD AC3/AC6 KO mice had similar arterial pressure and renal Na(+) and water handling compared with CD AC6 KO mice. In summary, these data do not support a significant role for CD AC3 in the regulation of renal Na(+) and water excretion in general or vasopressin regulation of CD function in particular.

Indexed as

Adenylyl CyclasesAnimalsBlood PressureDiuresisFemaleKidney Tubules, CollectingMaleMiceMice, KnockoutSodiumSodium Chloride, Dietaryadenylyl cyclase 6Adenylyl CyclasesSodiumSodium Chloride, Dietaryadenylyl cyclase 3blood pressurecollecting ductgene targetingurinary sodium and water excretion

Identifiers

PMID24431204
PMCPMC3949037
OpenAlexW2101119530

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.