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@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, roč.~67, č.~3, s.~339-351. ISSN~0867-5910. 2016.
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