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

Result code in 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>

Result on the web

<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>

Result language

angličtina

Original language name

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

Original language description

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.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

30104 - Pharmacology and pharmacy

Project

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Continuities

S - Specificky vyzkum na vysokych skolach

Publication year

2017

Confidentiality

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

Name of the periodical

Naunyn-Schmiedeberg's Archives of Pharmacology

ISSN

0028-1298

e-ISSN

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Volume of the periodical

390

Issue of the periodical within the volume

5

Country of publishing house

US - UNITED STATES

Number of pages

11

Pages from-to

471-481

UT code for WoS article

000399170600003

EID of the result in the Scopus database

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