Evidence map›Paper›PMID 2440506›Full record

ArticleBritish journal of pharmacology1987

Interaction of phorbol esters with Ca2+ channels in smooth muscle.

M Spedding

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 1987. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

6 citing papers in PubMed, 26 citations in OpenAlex.

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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

1 author at 1 institution in 1 country.

M Spedding
Synlab Czech (Czechia) · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA), a selective activator of protein kinase C, had no effect on the sensitivity to Ca2+ or verapamil of K+-depolarized taenia preparations from the guinea-pig caecum, despite the use of high concentrations (1 microM for 3 h); this preparation is sensitive to Ca2+ channel activators and antagonists. TPA (0.03-3 microM) caused a slow contraction of rat aorta preparations; the contractions were resistant to the calcium-antagonists nifedipine (0.01 microM), verapamil (10 microM), diltiazem (10 microM) and cinnarizine (10 microM), but were antagonized by N-(6-aminohexyl)-5-chloro-1-naphthalensulphonamide (W-7, 50-200 microM). Prolonged exposure to TPA (greater than 2 h) resulted in spontaneous contractions which were sensitive to verapamil (1 microM). Isoprenaline and sodium nitroprusside relaxed phenylephrine-induced contractions in rat aorta preparations. TPA (0.3 microM) blocked the maximal response to isoprenaline but not to sodium nitroprusside indicating that TPA did selectively activate protein kinase C under these experimental conditions. These findings indicate that protein kinase C activation does not result in direct effects on Ca2+ channel function, but may exert effects indirectly (e.g. by modifying intracellular sensitivity to Ca2+, Ca2+ extrusion, or cellular depolarization).

Indexed as

AnimalsAorta, ThoracicCalcium Channel BlockersCecumGuinea PigsIn Vitro TechniquesIon ChannelsMaleMuscle ContractionMuscle, SmoothPortal VeinPotassiumRatsRats, Inbred StrainsTetradecanoylphorbol AcetateCalcium Channel BlockersIon ChannelsPotassiumTetradecanoylphorbol Acetate

Identifiers

PMID2440506
PMCPMC1853522
OpenAlexW2039616077

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.