Evidence map›Paper›PMID 1330156›Full record

ArticleBritish journal of pharmacology1992

Cyclopiazonic acid, an inhibitor of the sarcoplasmic reticulum Ca(2+)-pump, reduces Ca(2+)-dependent K+ currents in guinea-pig smooth muscle cells.

M Suzuki, K Muraki, Y Imaizumi, M Watanabe

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 116 citations in OpenAlex.

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  4. Inhibitory effects of ginsenoside-rb2 on nicotinic stimulation-evoked catecholamine secretion.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2014
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  6. Group I mGluRs evoke K-ATP current by intracellular Ca2+ mobilization in rat subthalamus neurons.The Journal of pharmacology and experimental therapeutics · 2013
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  7. Influence of Fimasartan (a Novel AT(1) Receptor Blocker) on Catecholamine Release in the Adrenal Medulla of Spontaneously Hypertensive Rats.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2013
    Article
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  10. Inhibitory effects of olmesartan on catecholamine secretion from the perfused rat adrenal medulla.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2010
    Article
  11. Polyphenols of Rubus coreanum Inhibit Catecholamine Secretion from the Perfused Adrenal Medulla of SHRs.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2009
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  12. Effects of losartan on catecholamine release in the isolated rat adrenal gland.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2009
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  13. Provinol inhibits catecholamine secretion from the rat adrenal medulla.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2009
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  14. Resveratrol inhibits nicotinic stimulation-evoked catecholamine release from the adrenal medulla.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2008
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  15. Influence of ketamine on catecholamine secretion in the perfused rat adrenal medulla.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2008
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  16. Roles of dopaminergic d(1) and d(2) receptors in catecholamine release from the rat adrenal medulla.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2008
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  17. Article
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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

4 authors at 1 institution in 1 country.

M SuzukiDepartment of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Nagoya City University, Japan.
K Muraki
Y Imaizumi
M Watanabe
Nagoya City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Effects of cyclopiazonic acid (CPA), a specific inhibitor of the Ca(2+)-ATPase in sarcoplasmic reticulum (SR), on membrane ionic currents were examined in single smooth muscle cells freshly isolated from ileal longitudinal strips and urinary bladder of the guinea-pig. 2. Under whole-cell clamp, CPA (1-10 microM) reduced peak outward current elicited by depolarization in a concentration-dependent manner. The concentration of CPA required for 50% decrease in the peak outward current was approximately 3 microM in ileal cells under these conditions. The current reduced by CPA recovered by more than 70% after washout. 3. The transient outward current elicited by application of 5 mM caffeine at a holding potential of -50 mV in Ca2+ free solution was almost abolished, when the preceding Ca(2+)-loading of the cell in a solution containing 2.2 mM Ca2+ was performed in the presence of 3 microM CPA. 4. When the Ca(2+)-dependent K+ current (IK-Ca) and Ca2+ current (ICa) were inhibited by addition of Ca2+, the remaining delayed rectifier type K+ current was not affected by 10 microM CPA. When outward currents were blocked by replacement of K+ by Cs+ in the pipette solution, the remaining ICa was not affected by 10 microM CPA. 5. CPA (10 microM) did not affect the conductance of single maxi Ca(2+)-dependent K+ channels or the Cd(2+)-dependence of their open probability in both inside- and outside-out configurations. 6. These results indicate that IK-Ca is selectively and strongly suppressed by CPA.Its effects may be attributed to a decrease in Ca2"-uptake into SR, resulting in a decrease in Ca2"-induced Ca24 release which is triggered by Ca24 entering through voltage-dependent Ca24 channels and therefore less activation of these K channels.7. CPA may be extremely valuable pharmacological tool for investigating intracellular Ca24 mobilization and ionic currents regulated by intracellular Ca24.

Indexed as

AnimalsCalciumCalcium-Transporting ATPasesElectric ConductivityElectric StimulationGuinea PigsIleumIndolesIn Vitro TechniquesMuscle, SmoothPotassiumPotassium ChannelsSarcoplasmic ReticulumUrinary BladderCalciumCalcium-Transporting ATPasescyclopiazonic acidIndolesPotassiumPotassium Channels

Identifiers

PMID1330156
PMCPMC1907594
OpenAlexW1975747269

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.