Effect of ethanol at clinically relevant concentrations on atrial inward rectifier potassium current sensitive to acetylcholine

Kód výsledku v 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>

Nalezeny alternativní kódy

RIV/62157124:16370/16:43874204 RIV/00216224:14110/16:00088863

Výsledek na webu

<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>

Jazyk výsledku

angličtina

Název v původním jazyce

Effect of ethanol at clinically relevant concentrations on atrial inward rectifier potassium current sensitive to acetylcholine

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

Effect of ethanol at clinically relevant concentrations on atrial inward rectifier potassium current sensitive to acetylcholine

Popis výsledku anglicky

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.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

BO - Biofyzika

OECD FORD obor

—

Projekt

<a href="/cs/project/NT14301" target="_blank" >NT14301: Vliv ethanolu a jeho metabolitu acetaldehydu na srdeční inward rectifier draslíkové proudy: vztah k fibrilaci síní po konzumaci alkoholu?</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2016

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Naunyn-Schmiedeberg's Archives of Pharmacology

ISSN

0028-1298

e-ISSN

—

Svazek periodika

389

Číslo periodika v rámci svazku

10

Stát vydavatele periodika

DE - Spolková republika Německo

Počet stran výsledku

10

Strana od-do

1049-1058

Kód UT WoS článku

000383665800002

EID výsledku v databázi Scopus

2-s2.0-84976463480