Evidence map›Paper›PMID 23264685›Full record

ArticleJournal of the American Society of Nephrology : JASN2013

Adenylyl cyclase VI mediates vasopressin-stimulated ENaC activity.

Karl P Roos, Vladislav Bugaj, Elena Mironova, James D Stockand, Nirupama Ramkumar, Sara Rees, Donald E Kohan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Stimulation of the Epithelial NaFrontiers in physiology · 2021
    Article
  4. Article
  5. Journal of the American Society of Nephrology : JASN · 2020
    Article
  6. Review
  7. Article
  8. Renal NaAmerican journal of physiology. Renal physiology · 2019
    Article
  9. Article
  10. Adenylyl cyclase 6 is required for maintaining acid-base homeostasis.Clinical science (London, England : 1979) · 2018
    Article
  11. Net KKidney international · 2017
    Article
  12. Review
  13. Vasopressin/V2 receptor stimulates renin synthesis in the collecting duct.American journal of physiology. Renal physiology · 2016
    Article
  14. Article
  15. Prolactin stimulates sodium and chloride ion channels in A6 renal epithelial cells.American journal of physiology. Renal physiology · 2015
    Article
  16. Article
  17. Article
  18. Article
  19. Renal phosphate wasting in the absence of adenylyl cyclase 6.Journal of the American Society of Nephrology : JASN · 2014
    Article
  20. Regulation of nephron water and electrolyte transport by adenylyl cyclases.American journal of physiology. Renal physiology · 2014
    Review
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

7 authors at 3 institutions in 2 countries.

Karl P RoosDivision of Nephrology, University of Utah Health Sciences Center, Salt Lake City, UT 84132, USA.
Vladislav Bugaj
Elena Mironova
James D Stockand
Nirupama Ramkumar
Sara Rees
Donald E Kohan
University of Utah · USThe University of Texas Health Science Center at San Antonio · USLaboratoire d’immunologie intégrative du cancer · FR

Funding

Regulation of the epithelial Na+ channel by Ras and SgkR01DK059594 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI STOCKAND, JAMES D · 2002 to 2012
$2.7M
NIDDK NIH HHS R01 DK059594
6 · The paper itself

Abstract

Vasopressin modulates sodium reabsorption in the collecting duct through adenylyl cyclase-stimulated cyclic AMP, which exists as multiple isoforms; the specific isoform involved in vasopressin-stimulated sodium transport is unknown. To assess this, we studied mice deficient in adenylyl cyclase type VI specifically in the principal cells of the collecting duct. Knockout mice had increased urine volume and reduced urine sodium concentration, but regardless of the level of sodium intake, they did not exhibit significant alterations in urinary sodium excretion, arterial pressure, or pulse rate. Plasma renin concentration was elevated in knockout mice, however, suggesting a compensatory response. Valsartan significantly reduced arterial pressure in knockout mice but not in controls. Knockout mice had decreased renal cortical mRNA content of all three epithelial sodium channel (ENaC) isoforms, and total cell sodium channel isoforms α and γ were reduced in these animals. Patch-clamp analysis of split-open cortical collecting ducts revealed no difference in baseline activity of sodium channels, but knockout mice had abolished vasopressin-stimulated ENaC open probability and apical membrane channel number. In summary, these data suggest that adenylyl cyclase VI mediates vasopressin-stimulated ENaC activity in the kidney.

Indexed as

Adenylyl CyclasesAldosteroneAnimalsAntidiuretic AgentsAntihypertensive AgentsAquaporin 2Arginine VasopressinBlood PressureEpithelial Sodium ChannelsFemaleHeart RateKidney Tubules, CollectingMaleMiceMice, KnockoutPatch-Clamp Techniquesadenylyl cyclase 6Adenylyl CyclasesAldosteroneAntidiuretic AgentsAntihypertensive AgentsAqp2 protein, mouseAquaporin 2Arginine VasopressinEpithelial Sodium ChannelsReninScnn1a protein, mouseScnn1b protein, mouseScnn1g protein, mouseSodiumSodium Chloride, DietaryTetrazolesValineValsartan

Identifiers

PMID23264685
PMCPMC3559481
OpenAlexW2137964475

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.