Evidence map›Paper›PMID 26607172›Full record

ArticlePhysiological reports2015

Electrophysiological properties of myocytes isolated from the mouse atrioventricular node: L-type ICa, IKr, If, and Na-Ca exchange.

Stéphanie C Choisy, Hongwei Cheng, Clive H Orchard, Andrew F James, Jules C Hancox

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Small-conductance calcium-activated potassium channels in the heart: expression, regulation and pathological implications.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  5. Article
  6. 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

5 authors at 2 institutions in 1 country.

Stéphanie C ChoisySchool of Physiology and Pharmacology and Cardiovascular Research Laboratories, Biomedical Sciences Building, University of Bristol, Bristol, United Kingdom.
Hongwei ChengSchool of Physiology and Pharmacology and Cardiovascular Research Laboratories, Biomedical Sciences Building, University of Bristol, Bristol, United Kingdom.
Clive H OrchardSchool of Physiology and Pharmacology and Cardiovascular Research Laboratories, Biomedical Sciences Building, University of Bristol, Bristol, United Kingdom.
Andrew F JamesSchool of Physiology and Pharmacology and Cardiovascular Research Laboratories, Biomedical Sciences Building, University of Bristol, Bristol, United Kingdom.
Jules C HancoxSchool of Physiology and Pharmacology and Cardiovascular Research Laboratories, Biomedical Sciences Building, University of Bristol, Bristol, United Kingdom jules.hancox@bristol.ac.uk.
University of Bristol · GBBristol Laboratories (United Kingdom) · GB

Funding

British Heart Foundation PG/11/24/28818British Heart Foundation PG/11/97/29193British Heart Foundation PG/14/21/30673
6 · The paper itself

Abstract

The atrioventricular node (AVN) is a key component of the cardiac pacemaker-conduction system. This study investigated the electrophysiology of cells isolated from the AVN region of adult mouse hearts, and compared murine ionic current magnitude with that of cells from the more extensively studied rabbit AVN. Whole-cell patch-clamp recordings of ionic currents, and perforated-patch recordings of action potentials (APs), were made at 35-37°C. Hyperpolarizing voltage commands from -40 mV elicited a Ba(2+)-sensitive inward rectifier current that was small at diastolic potentials. Some cells (Type 1; 33.4 ± 2.2 pF; n = 19) lacked the pacemaker current, If, whilst others (Type 2; 34.2 ± 1.5 pF; n = 21) exhibited a clear If, which was larger than in rabbit AVN cells. On depolarization from -40 mV L-type Ca(2+) current, IC a,L, was elicited with a half maximal activation voltage (V0.5) of -7.6 ± 1.2 mV (n = 24). IC a,L density was smaller than in rabbit AVN cells. Rapid delayed rectifier (IK r) tail currents sensitive to E-4031 (5 μmol/L) were observed on repolarization to -40 mV, with an activation V0.5 of -10.7 ± 4.7 mV (n = 8). The IK r magnitude was similar in mouse and rabbit AVN. Under Na-Ca exchange selective conditions, mouse AVN cells exhibited 5 mmol/L Ni-sensitive exchange current that was inwardly directed negative to the holding potential (-40 mV). Spontaneous APs (5.2 ± 0.5 sec(-1); n = 6) exhibited an upstroke velocity of 37.7 ± 16.2 V/s and ceased following inhibition of sarcoplasmic reticulum Ca(2+) release by 1 μmol/L ryanodine, implicating intracellular Ca(2+) cycling in murine AVN cell electrogenesis.

Indexed as

atrioventricular nodeAVNAV nodecalcium‐currenthyperpolarization‐activated currentI C a,LI fI K rI NCXpacemakingrapid delayed rectifierryanodine

Identifiers

PMID26607172
PMCPMC4673654
OpenAlexW2174608892

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.