EFFECT OF ETHANOL AND ACETALDEHYDE AT CLINICALLY RELEVANT CONCENTRATIONS ON ATRIAL INWARD RECTIFIER POTASSIUM CURRENT I-K1 SEPARATE AND COMBINED EFFECT

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388998%3A_____%2F16%3A00461806" target="_blank" >RIV/61388998:_____/16:00461806 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/62157124:16370/16:43874556 RIV/00216224:14110/16:00088864

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

EFFECT OF ETHANOL AND ACETALDEHYDE AT CLINICALLY RELEVANT CONCENTRATIONS ON ATRIAL INWARD RECTIFIER POTASSIUM CURRENT I-K1 SEPARATE AND COMBINED EFFECT

Popis výsledku v původním jazyce

Atrial fibrillation is the most common arrhythmia at alcohol consumption. Its pathogenesis is complex, at least partly related to changes of cardiac inward rectifier potassium currents including IK1. Both ethanol and acetaldehyde have been demonstrated to considerably modify IK1 in rat ventricular myocytes. However, analogical data on the atrial IK1 are lacking. The present study aimed to analyse IK1 changes induced by ethanol and acetyldehyde in atrial myocytes. The experiments were performed by the whole cell patch-clamp technique at 23 1°C on enzymatically isolated rat and guinea-pig atrial myocytes as well as on expressed human Kir2.3 channels. Ethanol (8 – 80 mM) caused a dual effect on the atrial IK1 showing the steady-state activation in some cells but inhibition in others in agreement with the ventricular data; on average, the activation was observed (at 20 mM by 4.3 and 4.5% in rat and guinea-pig atrial myocytes, respectively). The effect slightly increased with depolarization above –60 mV. In contrast, the current through human Kir2.3 channels (prevailing atrial IK1 subunit) was inhibited in all measured cells. Unlike ethanol, acetaldehyde (3 μM) markedly inhibited the rat atrial IK1 (by 15.1%) in a voltage-independent manner, comparably to the rat ventricular IK1. The concurrent application of ethanol (20 mM) and acetaldehyde (3 μM) resulted in the steady-state IK1 activation by 2.1% on average. We conclude that ethanol and even more acetaldehyde affected IK1 at clinically relevant concentrations if applied separately. Their combined effect did not significantly differ from the effect of ethanol alone.

Název v anglickém jazyce

EFFECT OF ETHANOL AND ACETALDEHYDE AT CLINICALLY RELEVANT CONCENTRATIONS ON ATRIAL INWARD RECTIFIER POTASSIUM CURRENT I-K1 SEPARATE AND COMBINED EFFECT

Popis výsledku anglicky

Atrial fibrillation is the most common arrhythmia at alcohol consumption. Its pathogenesis is complex, at least partly related to changes of cardiac inward rectifier potassium currents including IK1. Both ethanol and acetaldehyde have been demonstrated to considerably modify IK1 in rat ventricular myocytes. However, analogical data on the atrial IK1 are lacking. The present study aimed to analyse IK1 changes induced by ethanol and acetyldehyde in atrial myocytes. The experiments were performed by the whole cell patch-clamp technique at 23 1°C on enzymatically isolated rat and guinea-pig atrial myocytes as well as on expressed human Kir2.3 channels. Ethanol (8 – 80 mM) caused a dual effect on the atrial IK1 showing the steady-state activation in some cells but inhibition in others in agreement with the ventricular data; on average, the activation was observed (at 20 mM by 4.3 and 4.5% in rat and guinea-pig atrial myocytes, respectively). The effect slightly increased with depolarization above –60 mV. In contrast, the current through human Kir2.3 channels (prevailing atrial IK1 subunit) was inhibited in all measured cells. Unlike ethanol, acetaldehyde (3 μM) markedly inhibited the rat atrial IK1 (by 15.1%) in a voltage-independent manner, comparably to the rat ventricular IK1. The concurrent application of ethanol (20 mM) and acetaldehyde (3 μM) resulted in the steady-state IK1 activation by 2.1% on average. We conclude that ethanol and even more acetaldehyde affected IK1 at clinically relevant concentrations if applied separately. Their combined effect did not significantly differ from the effect of ethanol alone.

Druh

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

CEP obor

BO - Biofyzika

OECD FORD obor

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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

Journal of Physiology and Pharmacology

ISSN

0867-5910

e-ISSN

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Svazek periodika

67

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

PL - Polská republika

Počet stran výsledku

13

Strana od-do

339-351

Kód UT WoS článku

000383528300002

EID výsledku v databázi Scopus

2-s2.0-84982957530