Evidence map›Paper›PMID 12672654›Full record

ArticleAmerican journal of physiology. Cell physiology2003

Substance P inhibits bicarbonate secretion from guinea pig pancreatic ducts by modulating an anion exchanger.

Peter Hegyi, Michael A Gray, Barry E Argent

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Mouse pancreatic ductal organoid culture as a relevant model to study exocrine pancreatic ion secretion.Laboratory investigation; a journal of technical methods and pathology · 2020
    Article
  4. Review
  5. Development of a polarized pancreatic ductular cell epithelium for physiological studies.Journal of applied physiology (Bethesda, Md. : 1985) · 2018
    Article
  6. Review
  7. CK2 is a key regulator of SLC4A2-mediated ClPflugers Archiv : European journal of physiology · 2017
    Article
  8. Role of CFTR in epithelial physiology.Cellular and molecular life sciences : CMLS · 2017
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Inhibition of protein kinase CK2 closes the CFTR Cl channel, but has no effect on the cystic fibrosis mutant deltaF508-CFTR.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2009
    Article
  16. Article
  17. Article
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

3 authors.

Peter HegyiDepartment of Physiological Sciences, University Medical School, Newcastle upon Tyne NE2 4HH, UK.
Michael A Gray
Barry E Argent

Funding

Wellcome Trust 068096
6 · The paper itself

Abstract

The stimulatory pathways controlling HCO3- secretion by the pancreatic ductal epithelium are well described. However, only a few data are available concerning inhibitory mechanisms, which may play an important role in the physiological control of the pancreas. The aim of this study was to investigate the cellular mechanism by which substance P (SP) inhibits pancreatic ductal HCO3- secretion. Small intra/interlobular ducts were isolated from the pancreas of guinea pigs. During overnight culture the ducts seal to form a closed sac. Transmembrane HCO3- fluxes were calculated from changes in intracellular pH (measured using the pH-sensitive dye BCECF) and the buffering capacity of the cells. We found that secretin can stimulate HCO3- secretion in guinea pig pancreatic ducts about fivefold and that this effect could be totally blocked by SP. The inhibitory effect of SP was relieved by spantide, an SP receptor antagonist. SP had no effect on the activity of basolateral Na+-HCO3- cotransporters and Na+/H+ exchangers. However, the peptide did inhibit a Cl--dependent HCO3- efflux (secretory) mechanism, most probably the Cl-/HCO3 exchanger on the apical membrane of the duct cell.

Indexed as

AnimalsBicarbonatesCell MembraneChloride-Bicarbonate AntiportersEpithelial CellsFluoresceinsGuinea PigsHydrogen-Ion ConcentrationNeural InhibitionNeurokinin-1 Receptor AntagonistsPancreasPancreatic DuctsReceptors, Neurokinin-1SecretinSubstance P2',7'-bis(carboxyethyl)-5(6)-carboxyfluoresceinBicarbonatesChloride-Bicarbonate AntiportersFluoresceinsNeurokinin-1 Receptor AntagonistsReceptors, Neurokinin-1SecretinspantideSubstance P

Identifiers

PMID12672654
PMCPMC6517286
OpenAlexW2076978195

What OpenQuestion holds

Textmetadata
LicenceTDM
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.