Evidence map›Paper›PMID 11850511›Full record

ArticleThe Journal of physiology2002

Chloride transport in microperfused interlobular ducts isolated from guinea-pig pancreas.

H Ishiguro, S Naruse, M Kitagawa, T Mabuchi, T Kondo, T Hayakawa, R M Case, M C Steward

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03686618 (A Phase II Study to Establish the Efficacy of Synthetic Human SecretiN in Human Acute Pancreatitis), which is not on this map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.9field-weighted citation impact, top 10% 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.

NCT03686618 phase2unknown statusnot on this mapstarted 2018, after this paper: background citation

A Phase II Study to Establish the Efficacy of Synthetic Human SecretiN in Human Acute Pancreatitis (SNAP) Study

TypeinterventionalSponsorChiRhoClin, Inc.Ran2018 to 2019Enrolled40ConditionsPancreatitis, AcuteArmsSecretin
3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Review
  3. WNK kinase is a vasoactive chloride sensor in endothelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Review
  5. Article
  6. Article
  7. ClAmerican journal of physiology. Cell physiology · 2020
    Review
  8. Review
  9. Article
  10. Modulation of ClScience signaling · 2018
    Article
  11. Article
  12. Article
  13. Role of CFTR in epithelial physiology.Cellular and molecular life sciences : CMLS · 2017
    Review
  14. Article
  15. Article
  16. Intracellular Cl- as a signaling ion that potently regulates Na+/HCO3- transporters.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  17. Article
  18. Transepithelial bicarbonate secretion: lessons from the pancreas.Cold Spring Harbor perspectives in medicine · 2012
    Article
  19. Review
  20. 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

8 authors at 2 institutions in 2 countries.

H IshiguroInternal Medicine II and Human Nutrition, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466 8550, Japan. ishiguro@htc.nagoya-u.ac.jp
S Naruse
M Kitagawa
T Mabuchi
T Kondo
T Hayakawa
R M Case
M C Steward
Nagoya University · JPUniversity of Manchester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Isolated interlobular ducts from the guinea-pig pancreas secrete a HCO3--rich fluid in response to secretin. To determine the role of Cl- transporters in this process, intracellular Cl- concentration ([Cl-]i) was measured in ducts loaded with the Cl--sensitive fluoroprobe, 6-methoxy-N-ethylquinolinium chloride (MEQ). [Cl-]i decreased when the luminal Cl- concentration was reduced. This effect was stimulated by forskolin, was not dependent on HCO3- and was not inhibited by application of the anion channel/transporter inhibitor H2DIDS to the luminal membrane. It is therefore attributed to a cAMP-stimulated Cl- conductance, probably the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel. [Cl-]i also decreased when the basolateral Cl- concentration was reduced. This effect was not stimulated by forskolin, was largely dependent on HCO3- and was inhibited by basolateral H2DIDS. It is therefore mediated mainly by Cl-/HCO3- exchange. With high Cl- and low HCO3- concentrations in the lumen, steady-state [Cl-]i was 25-35 mM in unstimulated cells. Stimulation with forskolin caused [Cl-]i to increase by approximately 4 mM due to activation of the luminal anion exchanger. With low Cl- and high HCO3- concentrations in the lumen to simulate physiological conditions, steady-state [Cl-]i was 10-15 mM in unstimulated cells. Upon stimulation with forskolin, [Cl-]i fell to approximately 7 mM due to increased Cl- efflux via the luminal conductance. We conclude that, during stimulation under physiological conditions, [Cl-]i decreases to very low levels in guinea-pig pancreatic duct cells, largely as a result of the limited capacity of the basolateral transporters for Cl- uptake. The resulting lack of competition from intracellular Cl- may therefore favour HCO3- secretion via anion conductances in the luminal membrane, possibly CFTR.

Indexed as

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic AcidAnimalsBiological TransportChloridesFemaleGuinea PigsHomeostasisIntracellular MembranesIn Vitro TechniquesOsmolar ConcentrationPancreatic DuctsPerfusion4,4'-Diisothiocyanostilbene-2,2'-Disulfonic AcidChloridesdihydro-DIDS

Identifiers

PMID11850511
PMCPMC2290131
OpenAlexW2122848305

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.