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

Kód výsledku v 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>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

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

Popis výsledku anglicky

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.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

ED - Fyziologie

OECD FORD obor

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Projekt

<a href="/cs/project/NT14301" target="_blank" >NT14301: Vliv ethanolu a jeho metabolitu acetaldehydu na srdeční inward rectifier draslíkové proudy: vztah k fibrilaci síní po konzumaci alkoholu?</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2015

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Physiological Research

ISSN

0862-8408

e-ISSN

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Svazek periodika

64

Číslo periodika v rámci svazku

6

Stát vydavatele periodika

CZ - Česká republika

Počet stran výsledku

5

Strana od-do

939-943

Kód UT WoS článku

000367547900016

EID výsledku v databázi Scopus

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