Detailed Information on Publication Record
2015
Acetaldehyde at Clinically Relevant Concentrations Inhibits Inward Rectifier Potassium Current I-K1 in Rat Ventricular Myocytes
BÉBAROVÁ, Markéta, Peter MATEJOVIČ, Milena ŠIMURDOVÁ and Jiří ŠIMURDABasic information
Original name
Acetaldehyde at Clinically Relevant Concentrations Inhibits Inward Rectifier Potassium Current I-K1 in Rat Ventricular Myocytes
Authors
BÉBAROVÁ, Markéta (203 Czech Republic, guarantor, belonging to the institution), Peter MATEJOVIČ (703 Slovakia, belonging to the institution), Milena ŠIMURDOVÁ (203 Czech Republic, belonging to the institution) and Jiří ŠIMURDA (203 Czech Republic, belonging to the institution)
Edition
Physiological Research, Praha, Fyziologický ústav AV ČR, 2015, 0862-8408
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
30105 Physiology
Country of publisher
Czech Republic
Confidentiality degree
není předmětem státního či obchodního tajemství
Impact factor
Impact factor: 1.643
RIV identification code
RIV/00216224:14110/15:00087452
Organization unit
Faculty of Medicine
UT WoS
000367547900016
Keywords in English
Acetaldehyde; Arrhythmias; Inward rectifier; IK1 inhibition; Rat ventricular myocytes
Tags
Tags
International impact, Reviewed
Změněno: 29/2/2016 11:23, Ing. Mgr. Věra Pospíšilíková
Abstract
V originále
Considering the effects of alcohol on cardiac electrical behaviour as well as the important role of the inward rectifier potassium current IK1 in arrhythmogenesis, this study was aimed at the effect of acetaldehyde, the primary metabolite of ethanol, on IK1 in rat ventricular myocytes. Acetaldehyde induced a reversible inhibition of IK1 with IC50 = 53.7 +/- 7.7 microM at -110 mV; a significant inhibition was documented even at clinically-relevant concentrations (at 3 microM by 13.1 +/- 3.0%). The inhibition was voltage-independent at physiological voltages above -90 mV. The IK1 changes under acetaldehyde may contribute to alcohol-induced alterations of cardiac electrophysiology, especially in individuals with a genetic defect of aldehyde dehydrogenase where the acetaldehyde level may be elevated.
Links
NT14301, research and development project |
|