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

Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F15%3A00087452" target="_blank" >RIV/00216224:14110/15:00087452 - isvavai.cz</a>
Result on the web
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DOI - Digital Object Identifier
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Result language
angličtina
Original language name
Acetaldehyde at Clinically Relevant Concentrations Inhibits Inward Rectifier Potassium Current I-K1 in Rat Ventricular Myocytes
Original language description
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.
Czech name
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Czech description
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Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
ED - Physiology
OECD FORD branch
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Project
<a href="/en/project/NT14301" target="_blank" >NT14301: Effect of ethanol and its principle metabolite acetaldehyde on cardiac inward rectifier potassium currents: a link to atrial fibrillation related to alcohol consumption?</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year
2015
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

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