Evidence map›Paper›PMID 1726794›Full record

ArticleThe Journal of physiology1991

Effects of 2,3-butanedione monoxime on whole-cell Ca2+ channel currents in single cells of the guinea-pig taenia caeci.

R J Lang, R J Paul

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Small-molecule inhibitors of myosin proteins.Future medicinal chemistry · 2013
    Review
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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

2 authors at 1 institution in 1 country.

R J LangDepartment of Physiology, Monash University, Clayton, Victoria, Australia.
R J Paul
Monash University · AU

Funding

TRANSCRIPTIONAL CONTROL OF CARDIAC MYOSINSP01HL022619 · NHLBI · UNIVERSITY OF CINCINNATI · PI SCHWARTZ, ARNOLD · 1985 to 2003
$6.1M
VASCULAR METABOLISM AND ITS RELATION TO FUNCTIONR01HL023240 · NHLBI · UNIVERSITY OF CINCINNATI · PI PAUL, RICHARD JEROME · 1985 to 1994
–
NHLBI NIH HHS HL22619NHLBI NIH HHS HL23240
6 · The paper itself

Abstract

1. The inhibitory actions of cadmium (Cd2+), nifedipine and 2,3-butanedione monoxime (BDM) on whole-cell Ca2+ channel currents in single cells of the guinea-pig taenia caeci were investigated using a single-electrode whole-cell voltage-clamp technique. 2. Calcium channel currents were isolated using pipette solutions containing Cs+, tetraethylammonium and ATP (3 mM). Ca2+ or Ba2+ (7.5 mM) in the bathing solution acted as the charge carrier during inward current flow. Ca2+ channel currents in 7.5 mM-Ba2+ (IBa) were recorded at potentials positive to -40 mV, were maximal near 0 mV and reversed near +60 mV. Ca2+ channel activation showed a sigmoidal relationship with potential, which was half-maximal at -13 mV. 3. Both the inward and outward flow of current was depressed and eventually blocked by 0.3-100 microM-Cd2+, 0.1-10 microM-nifedipine and 2-20 mM-BDM. Half-maximal blockade of IBa at 0 mV was achieved with approximately 3 microM-Cd2+, 1 microM-nifedipine and 10 microM-BDM. Steady-state activation curves were not affected by Cd2+ or BDM, but were shifted in the hyperpolarizing direction by nifedipine at concentrations > 1 microM. 4. Calcium channel currents in single cells and K+ contractures in intact strips were both blocked in a voltage-dependent manner. Steady-state inactivation curves (f infinity (V)) for IBa were shifted 20 mV in the hyperpolarizing direction by 0.3 microM-nifedipine and 4 mV by 10 mM-BDM. From these shifts a dissociation binding constant to inactivated Ca2+ channels for nifedipine was estimated as 78 nM, and for BDM, 5 mM. 5. At 10 microM Cd2+ produced a 43 +/- 6% (n = 3) block of the inward current at 0 mV when Ca2+ (7.5 mM) was the charge carrier (ICa), compared with the 36 +/- 3% block of IBa induced by 1 microM-Cd2+, consistent with the suggestion that Ca2+, Ba2+ and Cd2+ compete for the same binding site. In contrast, nifedipine (1 microM) and BDM (10 mM) blocked ICa more effectively than IBa. 6. Bay K 8644 (1.0 microM) increased Ca2+ channel currents two- to fourfold at all potentials due to a shift, of approximately 10 mV in the negative direction, of their activation curve and an equal shift in the positive direction of their inactivation curve. BDM (5-10 mM) could antagonize the action of Bay K 8644, shifting both curves back towards their control.(ABSTRACT TRUNCATED AT 400 WORDS)

Indexed as

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl esterAdenosine TriphosphateAnimalsBariumCadmiumCalcium ChannelsColonDiacetylElectrophysiologyGuinea PigsIn Vitro TechniquesMembrane PotentialsNifedipinePotassium3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl esteradenosine 5'-O-(3-thiotriphosphate)Adenosine TriphosphateBariumCadmiumCalcium ChannelsDiacetyldiacetylmonoximeNifedipinePotassium

Identifiers

PMID1726794
PMCPMC1181356
OpenAlexW2113305678

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.