Účinek haloperidolu na napěťově závislé iontové proudy srdce

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F04%3A00011470" target="_blank" >RIV/00216224:14110/04:00011470 - 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

Effect of haloperidol on voltage dependent cardiac ion channels

Popis výsledku v původním jazyce

Haloperidol is a neuroleptic agent effective in treatment of various psychiatric diseases. Cardiac arrhythmias have been associated with this therapy. We have investigated effects of haloperidol on cardiac sodium, potassium and calcium channels using whole cell patch-clamp method. 10 microM concentration of haloperidol was tested. In cardiomyocytes isolated from adult rat ventricles, haloperidol inhibited 95% of sodium current (INa) activated by 40 ms voltage pulses from -75 mV to -20 mV. The block of the transient outward potassium current (Ito) and current at the end of the pulse (IK,end) were measured by 300 ms voltage pulses from -75 mV to +40 mV. Haloperidol caused 80% block of Ito and 37% block of IK,end. In all cases the block was reversible. Further, we have investigated CaV1.2 L-type calcium channel transiently expressed in HEK 293 cells. Haloperidol inhibited approximately 58% of inward current amplitude measured in peak of IV relation. The inhibition was reversible and volta

Název v anglickém jazyce

Effect of haloperidol on voltage dependent cardiac ion channels

Popis výsledku anglicky

Haloperidol is a neuroleptic agent effective in treatment of various psychiatric diseases. Cardiac arrhythmias have been associated with this therapy. We have investigated effects of haloperidol on cardiac sodium, potassium and calcium channels using whole cell patch-clamp method. 10 microM concentration of haloperidol was tested. In cardiomyocytes isolated from adult rat ventricles, haloperidol inhibited 95% of sodium current (INa) activated by 40 ms voltage pulses from -75 mV to -20 mV. The block of the transient outward potassium current (Ito) and current at the end of the pulse (IK,end) were measured by 300 ms voltage pulses from -75 mV to +40 mV. Haloperidol caused 80% block of Ito and 37% block of IK,end. In all cases the block was reversible. Further, we have investigated CaV1.2 L-type calcium channel transiently expressed in HEK 293 cells. Haloperidol inhibited approximately 58% of inward current amplitude measured in peak of IV relation. The inhibition was reversible and volta

Druh

D - Stať ve sborníku

CEP obor

ED - Fyziologie

OECD FORD obor

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Projekt

<a href="/cs/project/GA305%2F04%2F1385" target="_blank" >GA305/04/1385: Modulační úloha sigma signalizace na elektromechanické vztahy izolovaného kardiomyocytu a srdce</a><br>

Návaznosti

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

Rok uplatnění

2004

Kód důvěrnosti údajů

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

Název statě ve sborníku

Membrane Channels, Transporters and Receptors

ISBN

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ISSN

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e-ISSN

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Počet stran výsledku

1

Strana od-do

54

Název nakladatele

Institute of Molecular Physiology and Genetics

Místo vydání

Bratislava

Místo konání akce

Smolenice

Datum konání akce

5. 6. 2004

Typ akce podle státní příslušnosti

WRD - Celosvětová akce

Kód UT WoS článku

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