Evidence map›Paper›PMID 8866360›Full record

ArticleThe Journal of physiology1996

Accumulation of intracellular HCO3- by Na(+)-HCO3- cotransport in interlobular ducts from guinea-pig pancreas.

H Ishiguro, M C Steward, A R Lindsay, R M Case

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
10.1field-weighted citation impact, top 1% 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

67 citing papers in PubMed, 174 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Expression of the regulated isoform of the electrogenic NaAmerican journal of physiology. Gastrointestinal and liver physiology · 2021
    Article
  5. Article
  6. Article
  7. Bicarbonate permeation through anion channels: its role in health and disease.Pflugers Archiv : European journal of physiology · 2020
    Review
  8. The apical NaJournal of cellular physiology · 2019
    Article
  9. Review
  10. Review
  11. Review
  12. Functional identification of protein phosphatase 1-binding consensus residues in NBCe1-B.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018
    Article
  13. Article
  14. Role of CFTR in epithelial physiology.Cellular and molecular life sciences : CMLS · 2017
    Review
  15. Ahcyl2 upregulates NBCe1-B via multiple serine residues of the PEST domain-mediated association.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016
    Article
  16. Article
  17. Article
  18. Review
  19. Cation-coupled bicarbonate transporters.Comprehensive Physiology · 2014
    Review
  20. Review

7 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

4 authors at 1 institution in 1 country.

H IshiguroSchool of Biological Sciences, University of Manchester, UK.
M C Steward
A R Lindsay
R M Case
University of Manchester · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

1. Short segments of interlobular duct were microdissected from guinea-pig pancreas following enzymatic digestion. After overnight culture, intracellular pH (pH1) and Na+ concentration ([Na+]i) were measured by microfluorometry in duct cells loaded with either the pH-sensitive fluoroprobe 2'7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF) or the sodium-binding benzofuran isophthalate (SBFI). 2. The transporters responsible for maintaining pHi above equilibrium were investigated by using the NH4Cl pulse technique to acid load the cells. In the absence of HCO3-/CO2, the recovery of pH1 was Na+ dependent, abolished by 0.2 mM amiloride and by 10 microM N-methyl-N-isobutylamiloride and was therefore attributed to Na(+)-H+ exchange. 3. In the presence of HCO3-/CO2, amiloride only partially inhibited the recovery from acid loading. The amiloride-insensitive component was abolished by 0.5 mM H2DIDS and unaffected by depletion of intracellular Cl- and was therefore attributed to Na(+)-HCO3- cotransport. 4. Stimulation with 10 nM secretin did not cause a significant change in pH1 despite a significant increase in HCO3- efflux. However, in the presence of secretin, addition of 0.5 mM H2DIDS caused a decline in pH1 that was three times more rapid than that obtained with 0.2 mM amiloride. 5. In secretin-stimulated ducts, Na+ uptake increased when HCO3-/CO2 was added to the bath and this increase was strongly inhibited by 0.5 mM H2DIDS. 6. We conclude that Na(+)-HCO3- cotransport contributes approximately 75% of the HCO3- taken up by guinea-pig pancreatic duct cells during stimulation with secretin. It is proposed that electrical coupling between HCO3- efflux at the luminal membrane and electrogenic Na(+)-HCO3- cotransport at the basolateral membrane explains why secretin causes little change in pH1.

Indexed as

AmilorideAnimalsBiological TransportFemaleFluoresceinsGuinea PigsHydrogen-Ion ConcentrationIon TransportMalePancreasRatsSodium2',7'-bis(carboxyethyl)-5(6)-carboxyfluoresceinAmilorideFluoresceinsSodium

Identifiers

PMID8866360
PMCPMC1160733
OpenAlexW2062805140

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.