Detailed Information on Publication Record
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.Basic information
Original name
Effect of ethanol and acetaldehyde at clinically relevant concentrations on atrial inward rectifier potassium current I-K1: Separate and combined effect
Authors
HOŘÁKOVÁ, Zuzana (203 Czech Republic, belonging to the institution), Peter MATEJOVIČ (203 Czech Republic, belonging to the institution), Michal PÁSEK (203 Czech Republic, belonging to the institution), Jan HOŠEK (203 Czech Republic, belonging to the institution), Milena ŠIMURDOVÁ (203 Czech Republic, belonging to the institution), Jiří ŠIMURDA (203 Czech Republic, belonging to the institution) and Markéta BÉBAROVÁ (203 Czech Republic, guarantor, belonging to the institution)
Edition
Journal of Physiology and Pharmacology, Krakow, Polish Physiological Society, 2016, 0867-5910
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
30105 Physiology
Country of publisher
Poland
Confidentiality degree
není předmětem státního či obchodního tajemství
Impact factor
Impact factor: 2.883
RIV identification code
RIV/00216224:14110/16:00088864
Organization unit
Faculty of Medicine
UT WoS
000383528300002
Keywords in English
alcohol consumption; atrial arrhythmias; inward rectifier; ethanol; acetaldehyde; combined effect
Tags
Tags
International impact, Reviewed
Změněno: 24/10/2016 14:34, Ing. Mgr. Věra Pospíšilíková
Abstract
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.
Links
| NT14301, research and development project |
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