Evidence map›Paper›PMID 8675644›Full record

ArticleThe Journal of clinical investigation1995

rENaC is the predominant Na+ channel in the apical membrane of the rat renal inner medullary collecting duct.

K A Volk, R D Sigmund, P M Snyder, F J McDonald, M J Welsh, J B Stokes

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.3field-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

9 citing papers in PubMed, 75 citations in OpenAlex.

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  6. Mice heterozygous for beta-ENaC deletion have defective potassium excretion.American journal of physiology. Renal physiology · 2006
    Article
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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 2 institutions in 1 country.

K A VolkDepartment of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242, USA.
R D Sigmund
P M Snyder
F J McDonald
M J Welsh
J B Stokes
Howard Hughes Medical Institute · USUniversity of Iowa · US

Funding

REGULATION OF K SECRETION BY CORTICAL COLLECTING TUBULER01DK025231 · NIDDK · UNIVERSITY OF IOWA · PI STOKES, JOHN B · 1986 to 1994
–
NIDDK NIH HHS DK-25231
6 · The paper itself

Abstract

The terminal nephron segment, the inner medullary collecting duct (IMCD), absorbs Na+ by an electrogenic process that involves the entry through an apical (luminal) membrane Na+ channel. To understand the nature of this Na+ channel, we employed the patch clamp technique on the apical membrane of primary cultures of rat IMCD cells grown on permeable supports. We found that all ion channels detected in the cell-attached configuration were highly selective for Na+ (Li+) over K+. The open/closed transitions showed slow kinetics, had a slope conductance of 6-11 pS, and were sensitive to amiloride and benzamil. Nonselective cation channels with a higher conductance (25-30 pS), known to be present in IMCD cells, were not detected in the cell-attached configuration, but were readily detected in excised patches. The highly selective channels had properties similar to the recently described rat epithelial Na+ channel complex, rENaC. We therefore asked whether rENaC mRNA was present in the IMCD. We detected mRNA for all three rENaC subunits in rat renal papilla and also in primary cultures of the IMCD. Either glucocorticoid hormone or mineralocorticoid hormone increased the amount of alpha-rENaC subunit mRNA but had no effect on the mRNA level of the beta-rENaC or gamma-rENaC subunits. From these data, taken in the context of other studies on the characteristics of Na+ selective channels and the distribution of rENaC mRNA, we conclude that steroid stimulated Na+ absorption by the IMCD is mediated primarily by Na+ channels having properties of the rENaC subunit complex.

Indexed as

AmilorideAnalysis of VarianceAnimalsBlotting, NorthernCell MembraneCells, CulturedGene ExpressionGlucocorticoidsHydrocortisoneIon Channel GatingKidney MedullaKidney Tubules, CollectingKineticsLithiumMacromolecular SubstancesMembrane PotentialsAmilorideGlucocorticoidsHydrocortisoneLithiumMacromolecular SubstancesMineralocorticoidsPotassiumRNA, MessengerSodiumSodium Channels

Identifiers

PMID8675644
PMCPMC185984
OpenAlexW2011349985

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.