Evidence map›Paper›PMID 8722560›Full record

ArticleThe Journal of general physiology1996

Ca2+ currents in cerebral artery smooth muscle cells of rat at physiological Ca2+ concentrations.

M Rubart, J B Patlak, M T Nelson

Abstract read
In one paragraph

Article in The Journal of general physiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing 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

58 citing papers in PubMed.

  1. Article
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  4. Intraluminal pressure elevates intracellular calcium and contracts CNS pericytes: Role of voltage-dependent calcium channels.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

3 authors.

M RubartDepartment of Pharmacology, University of Vermont, Burlington 05405, USA.
J B Patlak
M T Nelson

Funding

REGULATION OF CEREBRAL ARTERY DILATIONR01HL044455 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI NELSON, MARK T · 1991 to 2010
$3.9M
MODES OF SINGLE NA+ CHANNEL GATING DURING LATE CURRENTSR01AR037606 · NIAMS · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI PATLAK, JOSEPH B · 1986 to 1994
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SEX HORMONES, ION CHANNELS, &CORONARY ARTERY REACTIVITYR01HL051728 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI NELSON, MARK T · 1994 to 1997
–
NHLBI NIH HHS HL44455NHLBI NIH HHS HL51728NIAMS NIH HHS AR37606
6 · The paper itself

Abstract

Single Ca2+ channel and whole cell currents were measured in smooth muscle cells dissociated from resistance-sized (100-microns diameter) rat cerebral arteries. We sought to quantify the magnitude of Ca2+ channel currents and activity under the putative physiological conditions of these cells: 2 mM [Ca2+]o, steady depolarizations to potentials between -50 and -20 mV, and (where possible) without extrinsic channel agonists. Single Ca2+ channel conductance was measured over a broad range of Ca2+ concentrations (0.5-80 mM). The saturating conductance ranged from 1.5 pS at 0.5 mM to 7.8 pS at 80 mM, with a value of 3.5 pS at 2 mM Ca (unitary currents of 0.18 pA at -40 mV). Both single channel and whole cell Ca2+ currents were measured during pulses and at steady holding potentials. Ca2+ channel open probability and the lower limit for the total number of channels per cell were estimated by dividing the whole-cell Ca2+ currents by the single channel current. We estimate that an average cell has at least 5,000 functional channels with open probabilities of 3.4 x 10(-4) and 2 x 10(-3) at -40 and -20 mV, respectively. An average of 1-10 (-40 mV and -20 mV, respectively) Ca2+ channels are thus open at physiological potentials, carrying approximately 0.5 pA steady Ca2+ current at -30 mV. We also observed a very slow reduction in open probability during steady test potentials when compared with peak pulse responses. This 4-10-fold reduction in activity could not be accounted for by the channel's normal inactivation at our recording potentials between -50 and -20 mV, implying that an additional slow inactivation process may be important in regulating Ca2+ channel activity during steady depolarization.

Indexed as

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl esterAnimalsCalciumCalcium ChannelsCerebral ArteriesDose-Response Relationship, DrugFemaleMuscle, SmoothRatsRats, Sprague-Dawley3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl esterCalciumCalcium Channels

Identifiers

PMID8722560
PMCPMC2217006

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Registered trials

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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.