Pannexin-1 Deficient Mice Have an Increased Susceptibility for Atrial Fibrillation and Show a QT-Prolongation Phenotype.
| Autor: | Petric S; University Childrenx00B4;s Hospital Duesseldorf, Pediatric Cardiology, Duesseldorf, Germany., Klein S, Dannenberg L, Lahres T, Clasen L, Schmidt KG, Ding Z, Donner BC |
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| Jazyk: | angličtina |
| Zdroj: | Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology [Cell Physiol Biochem] 2016; Vol. 38 (2), pp. 487-501. Date of Electronic Publication: 2016 Feb 01. |
| DOI: | 10.1159/000438645 |
| Abstrakt: | Background/aims: Pannexin-1 (Panx1) is an ATP release channel that is ubiquitously expressed and coupled to several ligand-gated receptors. In isolated cardiac myocytes, Panx1 forms large conductance channels that can be activated by Ca2+ release from the sarcoplasmic reticulum. Here we characterized the electrophysiological function of these channels in the heart in vivo, taking recourse to mice with Panx1 ablation. Methods: Cardiac phenotyping of Panx1 knock-out mice (Panx1(-/-)) was performed by employing a molecular, cellular and functional approach, including echocardiography, surface and telemetric ECG recordings with QT analysis, physical stress testing and quantification of heart rate variability. In addition, an in vivo electrophysiological study entailed programmed electrical stimulation using an intracardiac octapolar catheter. Results: Panx1 deficiency results in a higher incidence of AV-block, delayed ventricular depolarisation, significant prolongation of QT- and rate corrected QT-interval and a higher incidence of atrial fibrillation after intraatrial burst stimulation. Conclusion: Panx1 seems to play an important role in murine cardiac electrophysiology and warrants further consideration in the context of hereditary forms of atrial fibrillation. (© 2016 The Author(s) Published by S. Karger AG, Basel.) |
| Databáze: | MEDLINE |
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