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Title of the item:

Sinus node-like pacemaker mechanisms regulate ectopic pacemaker activity in the adult rat atrioventricular ring

Title :
Sinus node-like pacemaker mechanisms regulate ectopic pacemaker activity in the adult rat atrioventricular ring
Authors :
Sunil Jit R. J. Logantha
Sanjay R. Kharche
Yu Zhang
Andrew J. Atkinson
Guoliang Hao
Mark R. Boyett
Halina Dobrzynski
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Subject Terms :
Medicine
Science
Source :
Scientific Reports, Vol 9, Iss 1, Pp 1-16 (2019)
Publisher :
Nature Publishing Group, 2019.
Publication Year :
2019
Collection :
LCC:Medicine
LCC:Science
Document Type :
article
File Description :
electronic resource
Language :
English
ISSN :
2045-2322
Relation :
https://doaj.org/toc/2045-2322
DOI :
10.1038/s41598-019-48276-0
Access URL :
https://doaj.org/article/528dfa53538c4e9eb2e94d8b77e5e113
Accession Number :
edsdoj.528dfa53538c4e9eb2e94d8b77e5e113
Academic Journal
Abstract In adult mammalian hearts, atrioventricular rings (AVRs) surround the atrial orifices of atrioventricular valves and are hotbed of ectopic activity in patients with focal atrial tachycardia. Experimental data offering mechanistic insights into initiation and maintenance of ectopic foci is lacking. We aimed to characterise AVRs in structurally normal rat hearts, identify arrhythmia predisposition and investigate mechanisms underlying arrhythmogenicity. Extracellular potential mapping and intracellular action potential recording techniques were used for electrophysiology, qPCR for gene and, Western blot and immunohistochemistry for protein expression. Conditions favouring ectopic foci were assessed by simulations. In right atrial preparations, sinus node (SN) was dominant and AVRs displayed 1:1 impulse conduction. Detaching SN unmasked ectopic pacemaking in AVRs and pacemaker action potentials were SN-like. Blocking pacemaker current I f, and disrupting intracellular Ca2+ release, prolonged spontaneous cycle length in AVRs, indicating a role for SN-like pacemaker mechanisms. AVRs labelled positive for HCN4, and SERCA2a was comparable to SN. Pacemaking was potentiated by isoproterenol and abolished with carbachol and AVRs had abundant sympathetic nerve endings. β2-adrenergic and M2-muscarinic receptor mRNA and β2-receptor protein were comparable to SN. In computer simulations of a sick SN, ectopic foci in AVR were unmasked, causing transient suppression of SN pacemaking.
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