J 2017

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

BÉBAROVÁ, Markéta, Peter MATEJOVIČ, Olga ŠVECOVÁ, Roman KULA, Milena ŠIMURDOVÁ et. al.

Základní údaje

Originální název

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

Autoři

BÉBAROVÁ, Markéta (203 Česká republika, garant, domácí), Peter MATEJOVIČ (203 Česká republika, domácí), Olga ŠVECOVÁ (643 Rusko, domácí), Roman KULA (203 Česká republika, domácí), Milena ŠIMURDOVÁ (203 Česká republika, domácí) a Jiří ŠIMURDA (203 Česká republika, domácí)

Vydání

Naunyn-Schmiedeberg's Archives of Pharmacology, New York, Springer, 2017, 0028-1298

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30104 Pharmacology and pharmacy

Stát vydavatele

Spojené státy

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 2.238

Kód RIV

RIV/00216224:14110/17:00096591

Organizační jednotka

Lékařská fakulta

UT WoS

000399170600003

Klíčová slova anglicky

Acetylcholine-sensitive; Dual effect; Inward rectifier; Nicotine

Štítky

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 20. 3. 2018 12:07, Soňa Böhmová

Anotace

V originále

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.

Návaznosti

MUNI/A/1365/2015, interní kód MU
Název: Kardiovaskulární systém: od modelu přes terapii k prevenci (Akronym: KAMOTEPRE)
Investor: Masarykova univerzita, Kardiovaskulární systém: od modelu přes terapii k prevenci, DO R. 2020_Kategorie A - Specifický výzkum - Studentské výzkumné projekty