Evidence map›Paper›PMID 12665604›Full record

ArticleThe Journal of physiology2003

Propagation of slow waves requires IP3 receptors and mitochondrial Ca2+ uptake in canine colonic muscles.

Sean M Ward, Salah A Baker, Andrew de Faoite, Kenton M Sanders

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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.

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

24 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Conditional deletion of IPJournal of gastroenterology · 2025
    Article
  3. Article
  4. Review
  5. CaPhysiological reviews · 2024
    Review
  6. CaCell calcium · 2021
    Article
  7. Bicarbonate ion transport by the electrogenic NaNeurogastroenterology and motility · 2021
    Article
  8. Deletion of IPJournal of gastroenterology · 2019
    Article
  9. Review
  10. Article
  11. Article
  12. Clustering of CaThe Journal of general physiology · 2017
    Article
  13. Review
  14. Mitochondrial calcium handling within the interstitial cells of Cajal.American journal of physiology. Gastrointestinal and liver physiology · 2014
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Sean M WardDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno 89557, USA. sean@physio.unr.edu
Salah A Baker
Andrew de Faoite
Kenton M Sanders
University of Nevada, Reno · US

Funding

Tissue, Cell and Tissue Culture CoreP01DK041315 · NIDDK · UNIVERSITY OF NEVADA RENO · PI WARD, SEAN M · 1989 to 2018
$26.3M
NIDDK NIH HHS DK 41315NIDDK NIH HHS P01 DK041315
6 · The paper itself

Abstract

In the gastrointestinal (GI) tract electrical slow waves yield oscillations in membrane potential that periodically increase the open probability of voltage-dependent Ca2+ channels and facilitate phasic contractions. Slow waves are generated by the interstitial cells of Cajal (ICC), and these events actively propagate through ICC networks within the walls of GI organs. The mechanism that entrains spontaneously active pacemaker sites throughout ICC networks to produce regenerative propagation of slow waves is unresolved. Agents that block inositol 1,4,5-trisphosphate (IP3) receptors and mitochondrial Ca2+ uptake were tested on the generation of slow waves in the canine colon. A partitioned chamber apparatus was used to test the effects of blocking slow-wave generation on propagation. We found that active propagation occurred along strips of colonic muscle, but when the pacemaker mechanism was blocked in a portion of the tissue, slow waves decayed exponentially from the point where the pacemaker mechanism was inhibited. An IP3 receptor inhibitor, mitochondrial inhibitors, low external Ca2+, and divalent cations (Mn2+ and Ni2+) caused exponential decay of the slow waves in regions of muscle exposed to these agents. These data demonstrate that the mechanism that initiates slow waves is reactivated from cell-to-cell during the propagation of slow waves. Voltage-dependent conductances present in smooth muscle cells are incapable of slow-wave regeneration. The data predict that partial loss of or disruptions to ICC networks observed in human motility disorders could lead to incomplete penetration of slow waves through GI organs and, thus, to defects in myogenic regulation.

Indexed as

AnimalsAntimycin ABoron CompoundsCalciumCalcium ChannelsCarbonyl Cyanide m-Chlorophenyl HydrazoneCarbonyl Cyanide p-TrifluoromethoxyphenylhydrazoneColonDogsFemaleGastrointestinal MotilityInositol 1,4,5-Trisphosphate ReceptorsMaleManganeseMembrane PotentialsMitochondria2-aminoethoxydiphenyl borateAntimycin ABoron CompoundsCalciumCalcium ChannelsCarbonyl Cyanide m-Chlorophenyl HydrazoneCarbonyl Cyanide p-TrifluoromethoxyphenylhydrazoneInositol 1,4,5-Trisphosphate ReceptorsITPR1 protein, humanManganeseNickelReceptors, Cytoplasmic and NuclearUncoupling Agents

Identifiers

PMID12665604
PMCPMC2342916
OpenAlexW1997587367

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.