Evidence map›Paper›PMID 17572704›Full record

ArticleBritish journal of pharmacology2007

Blockade of gap junction coupling by glycyrrhetinic acids in guinea pig cochlear artery: a whole-cell voltage- and current-clamp study.

B-C Guan, J-Q Si, Z-G Jiang

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2007. 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
1.3field-weighted citation impact, top 22% 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, 34 citations in OpenAlex.

  1. Mechanisms of Connexin-Related Lymphedema.Circulation research · 2018
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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 at 2 institutions in 2 countries.

B-C GuanDepartment of Otolaryngology, Oregon Hearing Research Center, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA.
J-Q Si
Z-G Jiang
Oregon Health & Science University · USShihezi University · CN

Funding

PORTLAND AREA COMMUNICATION RESEARCH CORE CENTERP30DC005983 · NIDCD · OREGON HEALTH & SCIENCE UNIVERSITY · PI NUTTALL, ALFRED L · 2003 to 2017
$9.0M
Cellular electrophysiology of vasculatures in inner earR01DC004716 · NIDCD · OREGON HEALTH & SCIENCE UNIVERSITY · PI JIANG, ZHI-GEN · 2003 to 2013
$2.8M
NIDCD NIH HHS DC 004716NIDCD NIH HHS P30 DC 005983NIDCD NIH HHS P30 DC005983NIDCD NIH HHS R01 DC004716
6 · The paper itself

Abstract

background and purposeGlycyrrhetinic acids (GAs) are widely used as gap junction blockers, but their efficacy and side effects have not been well determined. EXPERIMENTAL APPROACH: Whole-cell electrical recordings were made from vascular smooth muscle cells (VSMCs) embedded in or dissociated from, guinea pig cochlear artery segments. KEY

results18beta- & 18alpha-GA concentration-dependently increased membrane input resistance (R(in)) of in situ VSMCs, with a maximal input conductance (G(in)=1/R(in)) reduction of 92% & 77% and IC(50) of 2.0 & 4.4 microm, respectively. 18betaGA (30 microM) resulted in a R(in) of 2.2 GOmega and C(in) of 12 pF, comparable to those of freshly dissociated VSMCs (3.1 GOmega & 6.1 pF). The GAs (> or =30 microM) caused a depolarization in VSMCs in situ. In dispersed VSMCs, they both inhibited delayed rectifiers; 18betaGA also activated a non-selective cation conductance while 18alphaGA inactivated a voltage-independent K+-conductance. ACh induced an outward current in VSMCs in situ at -40 mV, with a positive slope I/V relation and a reversal potential near E(K). The ACh-induced current was attenuated by 18beta- & 18alphaGA with an IC(50) of 4.3 & 7.8 microM, respectively. CONCLUSIONS AND IMPLICATIONS: 18betaGA blocked the vascular gap junctions, achieving a complete electrical isolation of the recorded VSMC at > or =30 microM while causing a mild depolarization by a complex conductance alteration. 18betaGA suppressed the ACh-induced current in VSMC by blocking the myoendothelial gap junction and by a non-junctional action. 18alphaGA at 30-100 microM failed to fully block the gap junctions while exerting side actions.

Indexed as

4-AminopyridineAcetylcholineAnimalsArteriesBiological FactorsCochleaDelayed Rectifier Potassium ChannelsDose-Response Relationship, DrugElectric ConductivityGap JunctionsGlycyrrhetinic AcidGuinea PigsMembrane PotentialsMuscle, Smooth, VascularPatch-Clamp TechniquesPotassium18alpha-glycyrrhetinic acid4-AminopyridineAcetylcholineBiological FactorsDelayed Rectifier Potassium Channelsendothelium-dependent hyperpolarization factorGlycyrrhetinic AcidPotassiumPotassium Channels, Inwardly RectifyingTetraethylammonium

Identifiers

PMID17572704
PMCPMC2042944
OpenAlexW1585686121

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.