Abstract
Background: Adenosine provokes atrial fibrillation (AF) with a higher activation frequency in right atria (RA) versus left atria (LA) in patients, but the underlying molecular and functional substrates are unclear. We tested the hypothesis that adenosine-induced AF is driven by localized reentry in RA areas with highest expression of adenosine A1 receptor and its downstream GIRK (G protein-coupled inwardly rectifying potassium channels) channels (I K,Ado). Methods: We applied biatrial optical mapping and immunoblot mapping of various atrial regions to reveal the mechanism of adenosine-induced AF in explanted failing and nonfailing human hearts (n=37). Results: Optical mapping of coronary-perfused atria (n=24) revealed that adenosine perfusion (10-100 mol/L) produced more significant shortening of action potential durations in RA (from 290±45 to 239±41 ms, 17.3±10.4%; P
Original language | English (US) |
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Pages (from-to) | 486-498 |
Number of pages | 13 |
Journal | Circulation |
Volume | 134 |
Issue number | 6 |
DOIs | |
State | Published - Jul 2016 |
Keywords
- G protein-coupled inwardly rectifying potassium channels
- adenosine
- atrial fibrillation
- optical mapping
- receptor, adenosine A1
- tertiapin