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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

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    BO - Biophysics

  • OECD FORD branch

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

  • 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