Evidence map›Paper›PMID 8120836›Full record

ArticleThe Journal of physiology1993

Evidence for multiple open states of the Ca2+ channels in smooth muscle cells isolated from the guinea-pig detrusor.

S Nakayama, A F Brading

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 40 citations in OpenAlex.

  1. CaChannels (Austin, Tex.) · 2020
    Review
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  9. Anomalous L-type calcium channels of rat spinal motoneurons.The Journal of general physiology · 1999
    Article
  10. Electrophysiological properties of the bladder.International urogynecology journal and pelvic floor dysfunction · 1998
    Review
  11. Article
  12. Modulation of the cloned skeletal muscle L-type Ca2+ channel by anchored cAMP-dependent protein kinase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997
    Article
  13. Article
  14. 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

2 authors at 1 institution in 1 country.

S NakayamaUniversity Department of Pharmacology, Oxford.
A F Brading
University of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Whole-cell voltage clamp techniques were used to examine the properties of voltage-dependent Ca2+ channel currents in single smooth muscle cells enzymatically dissociated from guinea-pig urinary bladder. Potassium currents were blocked with intracellular Cs+. A holding potential of -60 mV was normally applied. 2. When the membrane potential was returned to the holding potential after a depolarizing step, tail currents were seen after depolarizations to positive potentials, and the size of the tail current increased with increasing positivity of the preceding depolarization. 3. After depolarization to +80 mV (a potential at which little inward current flowed through the Ca2+ channels) tail currents on returning to the holding potential increased in size as the duration of the depolarization was increased. 4. Investigation of the mechanism mediating the tail currents showed that they were not flowing through non-selective cation channels, and had no contribution from Ca(2+)-activated Cl- channels or Na(+)-Ca2+ exchange. 5. The tail currents and the inward currents evoked by a simple depolarizing test potential were equally decreased by nifedipine in a dose-dependent manner. This suggests that L-type Ca2+ channels are responsible for both of the two types of inward currents. The inward currents were also inhibited in a similar manner when caffeine was applied. 6. Although the tail currents evoked on stepping from +80 mV to a holding potential of -60 mV increased in size with the duration of the conditioning potential, the total membrane Ca2+ conductance did not increase, since the inward currents evoked on stepping to +20 mV (a potential at which the Ca2+ channels are still fully activated) did not change with time. 7. The amplitude of the inward current evoked by a simple depolarizing test potential was similar to that evoked on stepping to the same test potential after preconditioning at +80 mV, if the test potential was higher than +20 mV. However, following repolarization to the holding potential, the amplitude of the subsequent tail current was larger and the deactivation time constant longer, after the conditioning depolarization. These results suggest that the voltage-dependent Ca2+ channels have at least two open states with different time constants, the tail current being the result of a long open channel state induced by large depolarizations. 8. When variable repolarizing potentials were applied after n +80 mV depolarization (5 s), the current-voltage relationship of the tail current was nearly linear between -60 and +30 mV. The deactivation was faster when a larger repolarization step was applied.(ABSTRACT TRUNCATED AT 400 WORDS)

Indexed as

AnimalsCaffeineCalcium ChannelsChloride ChannelsEvoked PotentialsGuinea PigsIn Vitro TechniquesIon TransportKineticsMaleMembrane PotentialsModels, BiologicalMuscle, SmoothNifedipineTetrodotoxinUrinary BladderCaffeineCalcium ChannelsChloride ChannelsNifedipineTetrodotoxin

Identifiers

PMID8120836
PMCPMC1143953
OpenAlexW2002213265

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.