Evidence map›Paper›PMID 11790805›Full record

ArticleThe Journal of physiology2002

The role of the L-type Ca(2+) channel in refilling functional intracellular Ca(2+) stores in guinea-pig detrusor smooth muscle.

C Wu, G Sui, C H Fry

Abstract 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. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Ultrasound induces contraction of the bladder smooth muscle.International urology and nephrology · 2016
    Article
  7. Review
  8. T-type Ca2+ channels and the urinary and male genital tracts.Pflugers Archiv : European journal of physiology · 2014
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Electrophysiological properties of the bladder.International urogynecology journal and pelvic floor dysfunction · 1998
    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

3 authors.

C WuDepartment of Medicine, University College London, 48 Riding House Street, London W1W 7EY, UK.
G Sui
C H Fry

Funding

Wellcome Trust
6 · The paper itself

Abstract

The transient rise of intracellular Ca(2+) in detrusor smooth muscle cells is due to the release of Ca(2+) from intracellular stores. However, it is not known how store refilling is maintained at a constant level to ensure constancy of the contractile response. The aim of these experiments was to characterise the role of L-type Ca(2+) channels in refilling. Experiments used isolated guinea-pig detrusor myocytes and store Ca(2+) content was estimated by measuring the magnitude of change to the intracellular [Ca(2+)] ([Ca(2+)](i)) after application of caffeine or carbachol using epifluorescence microscopy. Membrane potential was controlled when necessary by voltage clamp. After Ca(2+) stores were emptied they refilled with an exponential time course, with a time constant of 88 s. The value of the time constant was similar to that of the undershoot of [Ca(2+)](i) following store Ca(2+) release. The degree of store filling was enhanced by maintained depolarisation, or by transient depolarising pulses, and attenuated by L-type Ca(2+) channel antagonists. Inhibition of the sarcoplasmic reticular Ca(2+)-ATPase prevented refilling. Reduction of the resting [Ca(2+)](i) was accompanied by membrane depolarisation; under voltage clamp reduction of [Ca(2+)](i) decreased the number and magnitude of spontaneous transient outward currents. Ca(2+) release from intracellular stores, elicited by caffeine or carbachol, is independent of membrane potential under physiological conditions. However, store refilling occurs via Ca(2+) influx through L-type Ca(2+) channels. Ca(2+) influx is regulated by a feedback mechanism whereby a fall of [Ca(2+)](i) reduces the activity of Ca(2+)-activated K(+) channels, causing cell depolarisation and an enhancement of L-type Ca(2+) channel conductance.

Indexed as

AnimalsCalciumCalcium Channel BlockersCalcium Channels, L-TypeCalcium-Transporting ATPasesCarbacholCholinergic AgonistsElectrophysiologyEnzyme InhibitorsGuinea PigsIndolesIntracellular MembranesMuscle ContractionMuscle, SmoothSarcoplasmic ReticulumUrinary BladderCalciumCalcium Channel BlockersCalcium Channels, L-TypeCalcium-Transporting ATPasesCarbacholCholinergic Agonistscyclopiazonic acidEnzyme InhibitorsIndoles

Identifiers

PMID11790805
PMCPMC2290076

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.