Evidence map›Paper›PMID 9423183›Full record

ArticleThe Journal of physiology1997

A functional CFTR protein is required for mouse intestinal cAMP-, cGMP- and Ca(2+)-dependent HCO3- secretion.

U Seidler, I Blumenstein, A Kretz, D Viellard-Baron, H Rossmann, W H Colledge, M Evans, R Ratcliff, M Gregor

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
9.3field-weighted citation impact, top 2% 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

78 citing papers in PubMed, 259 citations in OpenAlex.

  1. EMC3 is critical for CFTR function and calcium mobilization in the mouse intestinal epithelium.American journal of physiology. Gastrointestinal and liver physiology · 2025
    Article
  2. Bicarbonate secretion and acid/base sensing by the intestine.Pflugers Archiv : European journal of physiology · 2024
    Review
  3. Review
  4. Article
  5. Dietary NaCellular and molecular life sciences : CMLS · 2023
    Article
  6. Intestinal secretory mechanisms and diarrhea.American journal of physiology. Gastrointestinal and liver physiology · 2022
    Review
  7. Article
  8. The TRPA1 Agonist Cinnamaldehyde Induces the Secretion of HCOInternational journal of molecular sciences · 2021
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. NHERF3 is necessary forAmerican journal of physiology. Cell physiology · 2019
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. CaOncotarget · 2017
    Review

18 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

9 authors at 3 institutions in 2 countries.

U SeidlerI. Department of Medicine, Eberhard-Karls-Universität Tübingen, Germany. ursula.seidler@uni-tuebingen.de
I Blumenstein
A Kretz
D Viellard-Baron
H Rossmann
W H Colledge
M Evans
R Ratcliff
M Gregor
University of Tübingen · DEWellcome/Cancer Research UK Gurdon Institute · GBUniversity of Cambridge · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

1. Most segments of the gastrointestinal tract secrete HCO3-, but the molecular nature of the secretory mechanisms has not been identified. We had previously speculated that the regulator for intestinal electrogenic HCO3- secretion is the cystic fibrosis transmembrane regulator (CFTR) channel. To prove this hypothesis, we have now measured HCO3- secretion by pH-stat titration, and recorded the electrical parameters of in vitro duodenum, jejunum and ileum of mice deficient in the gene for the CFTR protein ('CF-mice') and their normal littermates. 2. Basal HCO3- secretory rates were reduced in all small intestinal segments of CF mice. Forskolin, PGE2, 8-bromo-cAMP and VIP (cAMP-dependent agonists), heat-stable enterotoxin of Escherichia coli (STa), guanylin and 8-bromo-cGMP (cGMP-dependent agonists) and carbachol (Ca2+ dependent) stimulated both the short-circuit current (Isc) and the HCO3- secretory rate (JHCO3-) in all intestinal segments in normal mice, whereas none of these agonists had any effect on JHCO3- in the intestine of CF mice. 3. To investigate whether Cl(-)-HCO3- exchangers, which have been implicated in mediating the response to some of these agonists in the intestine, were similarly active in the small intestine of normal and CF mice, we studied Cl- gradient-driven 36Cl- uptake into brush-border membrane (BBM) vesicles isolated from normal and CF mouse small intestine. Both the time course and the peak value for 4,4'-diisothiocyanostilbene-2',2-disulphonic acid (DIDS)-inhibited 36Cl- uptake was similar in normal and CF mice BBM vesicles. 4. In summary, the results demonstrate that the presence of the CFTR channel is necessary for agonist-induced stimulation of electrogenic HCO3- secretion in all segments of the small intestine, and all three intracellular signal transduction pathways stimulate HCO3- secretion exclusively via activation of the CFTR channel.

Indexed as

Gastrointestinal Hormones8-Bromo Cyclic Adenosine MonophosphateAnimalsBacterial ToxinsBicarbonatesCalciumCarbacholColforsinCyclic AMPCyclic GMPCystic Fibrosis Transmembrane Conductance RegulatorDinoprostoneDuodenumEnterotoxinsEscherichia coli ProteinsIleum8-Bromo Cyclic Adenosine Monophosphate8-bromocyclic GMPBacterial ToxinsBicarbonatesCalciumCarbacholColforsinCyclic AMPCyclic GMPCystic Fibrosis Transmembrane Conductance RegulatorDinoprostoneEnterotoxinsEscherichia coli ProteinsGastrointestinal Hormonesguanylinheat stable toxin (E coli)Natriuretic PeptidesPeptidesVasoactive Intestinal Peptide

Identifiers

PMID9423183
PMCPMC1160074
OpenAlexW2137012287

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.