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Adrenergic prolongation of action potential duration in rainbow trout myocardium via inhibition of the delayed rectifier potassium current, IKrстатья
Статья опубликована в высокорейтинговом журнале
Информация о цитировании статьи получена из
Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 8 апреля 2022 г.
- Авторы: Abramochkin Denis V., Haworth T.Eliot, Kuzmin Vladislav S., Dzhumaniiazova Irina, Pustovit Ksenia B., Gacoin Maeva, Shiels Holly A.
- Журнал: Comparative biochemistry and physiology. Part A, Molecular & integrative physiology
- Том: 267
- Год издания: 2022
- Издательство: Elsevier BV
- Местоположение издательства: Netherlands
- Номер статьи: 111161
- DOI: 10.1016/j.cbpa.2022.111161
- Аннотация: Catecholamines mediate the ‘fight or flight’ response in a wide variety of vertebrates. The endogenous catecholamineadrenaline increases heart rate and contractile strength to raise cardiac output. The increase incontractile force is driven in large part by an increase in myocyte Ca2+ influx on the L-type Ca current (ICaL)during the cardiac action potential (AP). Here, we report a K+- based mechanism that prolongs AP duration(APD) in fish hearts following adrenergic stimulation. We show that adrenergic stimulation inhibits the delayedrectifier K+ current (IKr) in rainbow trout (Oncorhynchus mykiss) cardiomyocytes. This slows repolarization andprolongs APD which may contribute to positive inotropy following adrenergic stimulation in fish hearts. Theendogenous ligand, adrenaline (1 μM), which activates both α- and β-ARs reduced maximal IKr tail current to61.4 ± 3.9% of control in atrial and ventricular myocytes resulting in an APD prolongation of ~20% at both 50and 90% repolarization. This effect was reproduced by the α-specific adrenergic agonist, phenylephrine (1 μM),but not the β-specific adrenergic agonist isoproterenol (1 μM). Adrenaline (1 μM) in the presence of β1 and β2-blockers (1 μM atenolol and 1 μM ICI-118551, respectively) also inhibited IKr. Thus, IKr suppression followingα-adrenergic stimulation leads to APD prolongation in the rainbow trout heart. This is the first time thismechanism has been identified in fish and may act in unison with the well-known enhancement of ICaL followingadrenergic stimulation to prolong APD and increase cardiac inotropy.
- Добавил в систему: Абрамочкин Денис Валерьевич