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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