Nicotine at clinically relevant concentrations affects atrial inward rectifier potassium current sensitive to acetylcholine

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F17%3A00096591" target="_blank" >RIV/00216224:14110/17:00096591 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1007/s00210-017-1341-z" target="_blank" >http://dx.doi.org/10.1007/s00210-017-1341-z</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1007/s00210-017-1341-z" target="_blank" >10.1007/s00210-017-1341-z</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Nicotine at clinically relevant concentrations affects atrial inward rectifier potassium current sensitive to acetylcholine

Popis výsledku v původním jazyce

Nicotine abuse is associated with variety of diseases including arrhythmias, most often atrial fibrillation (AF). Altered inward rectifier potassium currents including acetylcholine-sensitive current IK(Ach) are known to be related to AF pathogenesis. Since relevant data are missing, we aimed to investigate IK(Ach) changes at clinically relevant concentrations of nicotine. Experiments were performed by the whole cell patch clamp technique at 23 +/- 1 °C on isolated rat atrial myocytes. Nicotine was applied at following concentrations: 4, 40 and 400 nM; ethanol at 20 mM (0.09%). Nicotine at 40 and 400 nM significantly activated constitutively active component of IK(Ach) with the maximum effect at 40 nM (an increase by 100%); similar effect was observed at -110 and -50 mV. Changes at 4 nM nicotine were negligible on average. Coapplication of 40 nM nicotine and 20 mM ethanol (which is also known to activate this current) did not show cumulative effect. In the case of acetylcholine-induced component of IK(Ach), a dual effect of nicotine and its correlation with the current magnitude in control were apparent: the current was increased by nicotine in the cells showing small current in control and vice versa. The effect of 40 and 400 nM nicotine on acetylcholine-induced component of IK(Ach) was significantly different at -110 and -50 mV. We conclude that nicotine at clinically relevant concentrations significantly increased constitutively active component of IK(Ach) and showed a dual effect on its acetylcholine-induced component, similarly as ethanol. Synchronous application of nicotine and ethanol did not cause additive effect.

Název v anglickém jazyce

Nicotine at clinically relevant concentrations affects atrial inward rectifier potassium current sensitive to acetylcholine

Popis výsledku anglicky

Nicotine abuse is associated with variety of diseases including arrhythmias, most often atrial fibrillation (AF). Altered inward rectifier potassium currents including acetylcholine-sensitive current IK(Ach) are known to be related to AF pathogenesis. Since relevant data are missing, we aimed to investigate IK(Ach) changes at clinically relevant concentrations of nicotine. Experiments were performed by the whole cell patch clamp technique at 23 +/- 1 °C on isolated rat atrial myocytes. Nicotine was applied at following concentrations: 4, 40 and 400 nM; ethanol at 20 mM (0.09%). Nicotine at 40 and 400 nM significantly activated constitutively active component of IK(Ach) with the maximum effect at 40 nM (an increase by 100%); similar effect was observed at -110 and -50 mV. Changes at 4 nM nicotine were negligible on average. Coapplication of 40 nM nicotine and 20 mM ethanol (which is also known to activate this current) did not show cumulative effect. In the case of acetylcholine-induced component of IK(Ach), a dual effect of nicotine and its correlation with the current magnitude in control were apparent: the current was increased by nicotine in the cells showing small current in control and vice versa. The effect of 40 and 400 nM nicotine on acetylcholine-induced component of IK(Ach) was significantly different at -110 and -50 mV. We conclude that nicotine at clinically relevant concentrations significantly increased constitutively active component of IK(Ach) and showed a dual effect on its acetylcholine-induced component, similarly as ethanol. Synchronous application of nicotine and ethanol did not cause additive effect.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30104 - Pharmacology and pharmacy

Projekt

—

Návaznosti

S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2017

Kód důvěrnosti údajů

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

Název periodika

Naunyn-Schmiedeberg's Archives of Pharmacology

ISSN

0028-1298

e-ISSN

—

Svazek periodika

390

Číslo periodika v rámci svazku

5

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

11

Strana od-do

471-481

Kód UT WoS článku

000399170600003

EID výsledku v databázi Scopus

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