Please use this identifier to cite or link to this item: http://dx.doi.org/10.25673/37460
Title: Evidence for arrhythmogenic effects of A2A-adenosine receptors
Author(s): Boknik, Peter
Drzewiecki, Katharina
Eskandar, John
Gergs, UlrichLook up in the Integrated Authority File of the German National Library
Hofmann, BrittLook up in the Integrated Authority File of the German National Library
Treede, HendrikLook up in the Integrated Authority File of the German National Library
Grote-Wessels, Stephanie
Fabritz, Larissa
Kirchhof, PaulusLook up in the Integrated Authority File of the German National Library
Fortmüller, Lisa
Müller, Frank Ulrich
Schmitz, Wilhelm
Zimmermann, Norbert
Kirchhefer, UweLook up in the Integrated Authority File of the German National Library
Neumann, Joachim
Issue Date: 2019
Type: Article
Language: English
Abstract: Adenosine can be released from the heart and may stimulate four different cardiac adenosine receptors. A receptor subtype that couples to the generation of cyclic adenosine monophosphate (cAMP) is the A2A-adenosine receptor (A2A-AR). To better understand its role in cardiac function, we studied mechanical and electrophysiological effects in transgenic mice that overexpress the human A2A-AR in cardiomyocytes (A2A-TG). We used isolated preparations from the left atrium, the right atrium, isolated perfused hearts with surface electrocardiogram (ECG) recording, and surface body ECG recordings of living mice. The hypothesized arrhythmogenic effects of transgenicity per se and A2A-AR stimulation were studied. We noted an increase in the incidence of supraventricular and ventricular arrhythmias under these conditions in A2A-TG. Moreover, we noted that the A2A-AR agonist CGS 21680 exerted positive inotropic effect in isolated human electrically driven (1 Hz) right atrial trabeculae carneae. We conclude that A2A-ARs are functional not only in A2A-TG but also in isolated human atrial preparations. A2A-ARs in A2A-TG per se and their stimulation can lead to cardiac arrhythmias not only in isolated cardiac preparations from A2A-TG but also in living A2A-TG.
URI: https://opendata.uni-halle.de//handle/1981185920/37703
http://dx.doi.org/10.25673/37460
Open Access: Open access publication
License: (CC BY 4.0) Creative Commons Attribution 4.0(CC BY 4.0) Creative Commons Attribution 4.0
Sponsor/Funder: Publikationsfond MLU
Journal Title: Frontiers in pharmacology
Publisher: Frontiers Media
Publisher Place: Lausanne
Volume: 10
Issue: 1051
Original Publication: 10.3389/fphar.2019.01051
Appears in Collections:Open Access Publikationen der MLU

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