Effect of ethanol and acetaldehyde at clinically relevant
concentrations on atrial inward rectifier potassium current
I-K1: Separate and combined effect

J 2016

Effect of ethanol and acetaldehyde at clinically relevant concentrations on atrial inward rectifier potassium current I-K1: Separate and combined effect

HOŘÁKOVÁ, Zuzana, Peter MATEJOVIČ, Michal PÁSEK, Jan HOŠEK, Milena ŠIMURDOVÁ et. al.

Základní údaje

Originální název

Effect of ethanol and acetaldehyde at clinically relevant concentrations on atrial inward rectifier potassium current I-K1: Separate and combined effect

Autoři

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

Vydání

Journal of Physiology and Pharmacology, Krakow, Polish Physiological Society, 2016, 0867-5910

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30105 Physiology

Stát vydavatele

Polsko

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 2.883

Kód RIV

RIV/00216224:14110/16:00088864

Organizační jednotka

Lékařská fakulta

UT WoS

000383528300002

Klíčová slova anglicky

alcohol consumption; atrial arrhythmias; inward rectifier; ethanol; acetaldehyde; combined effect

Štítky

EL OK

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 24. 10. 2016 14:34, Ing. Mgr. Věra Pospíšilíková

Anotace

V originále

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 I-K1. Both ethanol and acetaldehyde have been demonstrated to considerably modify I-K1 in rat ventricular myocytes. However, analogical data on the atrial I-K1 are lacking. The present study aimed to analyse I-K1 changes induced by ethanol and acetyldehyde in atrial myocytes. The experiments were performed by the whole cell patch-clamp technique at 23 +/- 1 degrees 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 I-k1 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 I-K1 subunit) was inhibited in all measured cells. Unlike ethanol, acetaldehyde (3 mu M) markedly inhibited the rat atrial I-K1 (by 15.1%) in a voltage-independent manner, comparably to the rat ventricular I-K1. The concurrent application of ethanol (20 mM) and acetaldehyde (3 mu M) resulted in the steady-state I-K1 activation by 2.1% on average. We conclude that ethanol and even more acetaldehyde affected I-K1 at clinically relevant concentrations if applied separately. Their combined effect did not significantly differ from the effect of ethanol alone.

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?

Citovat

HOŘÁKOVÁ, Zuzana, Peter MATEJOVIČ, Michal PÁSEK, Jan HOŠEK, Milena ŠIMURDOVÁ, Jiří ŠIMURDA a Markéta BÉBAROVÁ. Effect of ethanol and acetaldehyde at clinically relevant concentrations on atrial inward rectifier potassium current I-K1: Separate and combined effect. Journal of Physiology and Pharmacology. Krakow: Polish Physiological Society, 2016, roč. 67, č. 3, s. 339-351. ISSN 0867-5910.

@article{1348899,
   author = {Hořáková, Zuzana and Matejovič, Peter and Pásek, Michal and Hošek, Jan and Šimurdová, Milena and Šimurda, Jiří and Bébarová, Markéta},
   article_location = {Krakow},
   article_number = {3},
   keywords = {alcohol consumption; atrial arrhythmias; inward rectifier; ethanol; acetaldehyde; combined effect},
   language = {eng},
   issn = {0867-5910},
   journal = {Journal of Physiology and Pharmacology},
   title = {Effect of ethanol and acetaldehyde at clinically relevant concentrations on atrial inward rectifier potassium current I-K1: Separate and combined effect},
   volume = {67},
   year = {2016}
}

TY  - JOUR
ID  - 1348899
AU  - Hořáková, Zuzana - Matejovič, Peter - Pásek, Michal - Hošek, Jan - Šimurdová, Milena - Šimurda, Jiří - Bébarová, Markéta
PY  - 2016
TI  - Effect of ethanol and acetaldehyde at clinically relevant concentrations on atrial inward rectifier potassium current I-K1: Separate and combined effect
JF  - Journal of Physiology and Pharmacology
VL  - 67
IS  - 3
SP  - 339-351
EP  - 339-351
PB  - Polish Physiological Society
SN  - 08675910
KW  - alcohol consumption
KW  - atrial arrhythmias
KW  - inward rectifier
KW  - ethanol
KW  - acetaldehyde
KW  - combined effect
N2  - 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 I-K1. Both ethanol and acetaldehyde have been demonstrated to considerably modify I-K1 in rat ventricular myocytes. However, analogical data on the atrial I-K1 are lacking. The present study aimed to analyse I-K1 changes induced by ethanol and acetyldehyde in atrial myocytes. The experiments were performed by the whole cell patch-clamp technique at 23 +/- 1 degrees 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 I-k1 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 I-K1 subunit) was inhibited in all measured cells. Unlike ethanol, acetaldehyde (3 mu M) markedly inhibited the rat atrial I-K1 (by 15.1%) in a voltage-independent manner, comparably to the rat ventricular I-K1. The concurrent application of ethanol (20 mM) and acetaldehyde (3 mu M) resulted in the steady-state I-K1 activation by 2.1% on average. We conclude that ethanol and even more acetaldehyde affected I-K1 at clinically relevant concentrations if applied separately. Their combined effect did not significantly differ from the effect of ethanol alone.
ER  -

HOŘÁKOVÁ, Zuzana, Peter MATEJOVIČ, Michal PÁSEK, Jan HOŠEK, Milena ŠIMURDOVÁ, Jiří ŠIMURDA a Markéta BÉBAROVÁ. Effect of ethanol and acetaldehyde at clinically relevant concentrations on atrial inward rectifier potassium current I-K1: Separate and combined effect. \textit{Journal of Physiology and Pharmacology}. Krakow: Polish Physiological Society, 2016, roč.~67, č.~3, s.~339-351. ISSN~0867-5910.

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