Evidence map›Paper›PMID 19478095›Full record

ArticleJournal of the American Society of Nephrology : JASN2009

Connexin 30 deficiency impairs renal tubular ATP release and pressure natriuresis.

Arnold Sipos, Sarah L Vargas, Ildikó Toma, Fiona Hanner, Klaus Willecke, János Peti-Peterdi

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

75 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
  2. Observational
  3. Calcium Regulation of Connexin Hemichannels.International journal of molecular sciences · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Connexin mRNA distribution in adult mouse kidneys.Pflugers Archiv : European journal of physiology · 2021
    Article
  11. Review
  12. Adenosine inhibits the basolateral ClAmerican journal of physiology. Renal physiology · 2020
    Article
  13. Article
  14. Review
  15. Review
  16. Renal NaAmerican journal of physiology. Renal physiology · 2019
    Article
  17. Article
  18. Article
  19. ATP Release Channels.International journal of molecular sciences · 2018
    Review
  20. Article

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

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

6 authors at 1 institution in 1 country.

Arnold SiposDepartment of Physiology and Biophysics and Department of Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, CA 90033, USA.
Sarah L Vargas
Ildikó Toma
Fiona Hanner
Klaus Willecke
János Peti-Peterdi
University of Southern California · US

Funding

Multiphoton Imaging of the Juxtaglomerular ApparatusR01DK064324 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JANOS PETI-PETERDI · 2004 to 2026
$8.4M
NIDDK NIH HHS DK64324NIDDK NIH HHS R01 DK064324
6 · The paper itself

Abstract

In the renal tubule, ATP is an important regulator of salt and water reabsorption, but the mechanism of ATP release is unknown. Several connexin (Cx) isoforms form mechanosensitive, ATP-permeable hemichannels. We localized Cx30 to the nonjunctional apical membrane of cells in the distal nephron and tested whether Cx30 participates in physiologically important release of ATP. We dissected, partially split open, and microperfused cortical collecting ducts from wild-type and Cx30-deficient mice in vitro. We used PC12 cells as ATP biosensors by loading them with Fluo-4/Fura Red to measure cytosolic calcium and positioning them in direct contact with the apical surface of either intercalated or principal cells. ATP biosensor responses, triggered by increased tubular flow or by bath hypotonicity, were approximately three-fold greater when positioned next to intercalated cells than next to principal cells. In addition, these responses did not occur in preparations from Cx30-deficient mice or with purinergic receptor blockade. After inducing step increases in mean arterial pressure by ligating the distal aorta followed by the mesenteric and celiac arteries, urine output increased 4.2-fold in wild-type mice compared with 2.6-fold in Cx30-deficient mice, and urinary Na(+) excretion increased 5.2-fold in wild-type mice compared with 2.8-fold in Cx30-deficient mice. Furthermore, Cx30-deficient mice developed endothelial sodium channel-dependent, salt-sensitive elevations in mean arterial pressure. Taken together, we suggest that mechanosensitive Cx30 hemichannels have an integral role in pressure natriuresis by releasing ATP into the tubular fluid, which inhibits salt and water reabsorption.

Indexed as

NatriuresisAdenosine TriphosphateAnimalsConnexin 30ConnexinsEpithelial Sodium ChannelsKidney Tubules, CollectingMiceMice, Inbred C57BLMice, KnockoutPressureReceptors, PurinergicAdenosine TriphosphateConnexin 30ConnexinsEpithelial Sodium ChannelsGjb6 protein, mouseReceptors, Purinergic

Identifiers

PMID19478095
PMCPMC2723976
OpenAlexW2114436085

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.