Effect of ethanol at clinically relevant concentrations on atrial inward rectifier potassium current sensitive to acetylcholine
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388998%3A_____%2F16%3A00462452" target="_blank" >RIV/61388998:_____/16:00462452 - isvavai.cz</a>
Alternative codes found
RIV/62157124:16370/16:43874204 RIV/00216224:14110/16:00088863
Result on the web
<a href="http://dx.doi.org/10.1007/s00210-016-1265-z" target="_blank" >http://dx.doi.org/10.1007/s00210-016-1265-z</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1007/s00210-016-1265-z" target="_blank" >10.1007/s00210-016-1265-z</a>
Alternative languages
Result language
angličtina
Original language name
Effect of ethanol at clinically relevant concentrations on atrial inward rectifier potassium current sensitive to acetylcholine
Original language description
Alcohol intoxication tends to induce arrhythmias, most often the atrial fibrillation. To elucidate arrhythmogenic mechanisms related to alcohol consumption, the effect of ethanol on main components of the ionic membrane current is investigated step by step. Considering limited knowledge, we aimed to examine the effect of clinically relevant concentrations of ethanol (0.8–80 mM) on acetylcholinesensitive inward rectifier potassium current IK(Ach). Experiments were performed by the whole-cell patch clamp technique at 23 1 °C on isolated rat and guinea-pig atrial myocytes, and on expressed human Kir3.1/3.4 channels. Ethanol induced changes of IK(Ach) in the whole range of concentrations applied; the effect was not voltage dependent. The constitutively active component of IK(Ach) was significantly increased by ethanol with the maximum effect (an increase by ∼100 %) between 8 and 20 mM. The changes were comparable in rat and guinea-pig atrial myocytes and also in expressed human Kir3.1/3.4 channels (i.e., structural correlate of IK(Ach)). In the case of the acetylcholine-induced component of IK(Ach), a dual ethanol effect was apparent with a striking heterogeneity of changes in individual cells. The effect correlated with the current magnitude in control: the current was increased by ethanol in the cells showing small current in control and vice versa. The average effect peaked at 20 mM ethanol (an increase of the current by ∼20 %). Observed changes of action potential duration agreed well with the voltage clamp data. Ethanol significantly affected both components of IK(Ach) even in concentrations corresponding to light alcohol consumption.
Czech name
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Czech description
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Classification
Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
BO - Biophysics
OECD FORD branch
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Result continuities
Project
<a href="/en/project/NT14301" target="_blank" >NT14301: Effect of ethanol and its principle metabolite acetaldehyde on cardiac inward rectifier potassium currents: a link to atrial fibrillation related to alcohol consumption?</a><br>
Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2016
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Naunyn-Schmiedeberg's Archives of Pharmacology
ISSN
0028-1298
e-ISSN
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Volume of the periodical
389
Issue of the periodical within the volume
10
Country of publishing house
DE - GERMANY
Number of pages
10
Pages from-to
1049-1058
UT code for WoS article
000383665800002
EID of the result in the Scopus database
2-s2.0-84976463480