J 2016

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

BÉBAROVÁ, Markéta, Peter MATEJOVIČ, Michal PÁSEK, Zuzana HOŘÁKOVÁ, Jan HOŠEK et. al.

Základní údaje

Originální název

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

Autoři

BÉBAROVÁ, Markéta (203 Česká republika, garant, domácí), Peter MATEJOVIČ (203 Česká republika, domácí), Michal PÁSEK (203 Česká republika, domácí), Zuzana HOŘÁKOVÁ (203 Česká republika, domácí), Jan HOŠEK (203 Česká republika, domácí), Milena ŠIMURDOVÁ (203 Česká republika, domácí) a Jiří ŠIMURDA (203 Česká republika, domácí)

Vydání

Naunyn-Schmiedeberg's Archives of Pharmacology, New York, Springer, 2016, 0028-1298

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30105 Physiology

Stát vydavatele

Spojené státy

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 2.558

Kód RIV

RIV/00216224:14110/16:00088863

Organizační jednotka

Lékařská fakulta

UT WoS

000383665800002

Klíčová slova anglicky

Ethanol; Inward rectifier; Dual effect; Kir3.1/3.4; Rat atrial cellmodel

Štítky

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 14. 11. 2016 10:39, Ing. Mgr. Věra Pospíšilíková

Anotace

V originále

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 acetylcholine-sensitive inward rectifier potassium current I (K(Ach)). Experiments were performed by the whole-cell patch clamp technique at 23 +/- 1 A degrees C on isolated rat and guinea-pig atrial myocytes, and on expressed human Kir3.1/3.4 channels. Ethanol induced changes of I (K(Ach)) in the whole range of concentrations applied; the effect was not voltage dependent. The constitutively active component of I (K(Ach)) was significantly increased by ethanol with the maximum effect (an increase by similar to 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 I (K(Ach))). In the case of the acetylcholine-induced component of I (K(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 eth-anol 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 similar to 20 %). Observed changes of action potential duration agreed well with the voltage clamp data. Ethanol significantly affected both components of I (K(Ach)) even in concentrations corresponding to light alcohol consumption.

Návaznosti

NT14301, projekt VaV
Název: Vliv ethanolu a jeho metabolitu acetaldehydu na srdeční inward rectifier draslíkové proudy: vztah k fibrilaci síní po konzumaci alkoholu?
Investor: Ministerstvo zdravotnictví ČR, Vliv ethanolu a jeho metabolitu acetaldehydu na srdeční inward rectifier draslíkové proudy: vztah k fibrilaci síní po konzumaci alkoholu?