Acetaldehyde at Clinically Relevant Concentrations Inhibits Inward Rectifier Potassium Current I-K1 in Rat Ventricular Myocytes

BÉBAROVÁ, Markéta, Peter MATEJOVIČ, Milena ŠIMURDOVÁ and Jiří ŠIMURDA. Acetaldehyde at Clinically Relevant Concentrations Inhibits Inward Rectifier Potassium Current I-K1 in Rat Ventricular Myocytes. Physiological Research. Praha: Fyziologický ústav AV ČR, 2015, vol. 64, No 6, p. 939-943. ISSN 0862-8408.

Basic 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

• Original language: English
• Type of outcome: Article in a journal
• Field of Study: 30105 Physiology
• Country of publisher: Czech Republic
• Confidentiality degree: is not subject to a state or trade secret
• 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: EL OK
• Tags: International impact, Reviewed

Abstract

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: Name: Vliv ethanolu a jeho metabolitu acetaldehydu na srdeční inward rectifier draslíkové proudy: vztah k fibrilaci síní po konzumaci alkoholu?

Investor: Ministry of Health of the CR