Dobromir Dobrev

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BACKGROUND The molecular mechanism of increased background inward rectifier current (IK1) in atrial fibrillation (AF) is not fully understood. We tested whether constitutively active acetylcholine (ACh)-activated I(K,ACh) contributes to enhanced basal conductance in chronic AF (cAF). METHODS AND RESULTS Whole-cell and single-channel currents were measured(More)
American Heart Association. All rights reserved. Print ISSN: 1941-3149. Online ISSN: 2008 Copyright © Greenville Avenue, Dallas, TX 72514 Circulation: Arrhythmia and Electrophysiology is published by the American Heart Association. 7272 DOI: 10.1161/CIRCEP.107.754564 2008;1;62-73; Circ Arrhythm Electrophysiol Stanley Nattel, Brett Burstein and Dobromir(More)
Atrial fibrillation (AF) is an extremely common cardiac rhythm disorder that causes substantial morbidity and contributes to mortality. The mechanisms underlying AF are complex, involving both increased spontaneous ectopic firing of atrial cells and impulse reentry through atrial tissue. Over the past ten years, there has been enormous progress in(More)
RATIONALE Understanding atrial fibrillation (AF) requires integrated understanding of ionic currents and Ca2+ transport in remodeled human atrium, but appropriate models are limited. OBJECTIVE To study AF, we developed a new human atrial action potential (AP) model, derived from atrial experimental results and our human ventricular myocyte model. (More)
A trial fibrillation (AF), the most common human cardiac arrhythmia, is associated with abnormal intracellular Ca2+ handling. Diastolic Ca2+ release from the sarcoplasmic reticulum via "leaky" ryanodine receptors (RyR2s) is hypothesized to contribute to arrhythmogenesis in AF, but the molecular mechanisms are incompletely understood. Here, we have shown(More)
Division of Experimental Cardiology, Dept of Experimental & Clinical Pharmacology, Medical Faculty Mannheim, University of Heidelberg, Mannheim; Dept of Pharmacology & Toxicology, Dresden University of Technology, Dresden, Germany; Dept of Molecular Physiology & Biophysics, Dept of Medicine, Baylor College of Medicine, Houston, TX; Unit of Cardiac(More)
BACKGROUND Clinical and experimental evidence suggest that the parasympathetic nervous system is involved in the pathogenesis of atrial fibrillation (AF). However, it is unclear whether changes in G-protein-coupled inward rectifying K(+) current (I(K,ACh)) contribute to chronic AF. METHODS AND RESULTS In the present study, we used electrophysiological(More)
BACKGROUND Delayed afterdepolarizations (DADs) carried by Na(+)-Ca(2+)-exchange current (I(NCX)) in response to sarcoplasmic reticulum (SR) Ca(2+) leak can promote atrial fibrillation (AF). The mechanisms leading to delayed afterdepolarizations in AF patients have not been defined. METHODS AND RESULTS Protein levels (Western blot), membrane currents and(More)
Sphingosine-1-phosphate (SPP) and sphingosylphosphorylcholine (SPPC) have been reported to activate muscarinic receptor-activated inward rectifier K(+) current (I(K.ACh)) in cultured guinea pig atrial myocytes with similar nanomolar potency. Members of the endothelial differentiation gene (Edg) receptor family were recently identified as receptors for SPP;(More)