Research article summary (published 15 Sep 2009):

Ultrastructural and functional remodeling of the coupling between Ca2+ influx and sarcoplasmic reticulum Ca2+ release in right atrial myocytes from experimental persistent atrial fibrillation.

Full Abstract

RATIONALE: Persistent atrial fibrillation (AF) has been associated with structural and electric remodeling and reduced contractile function. Objective: To unravel mechanisms underlying reduced sarcoplasmic reticulum (SR) Ca(2+) release in persistent AF. METHODS: We studied cell shortening, membrane currents, and [Ca(2+)](i) in right atrial myocytes isolated from sheep with persistent AF (duration 129+/-39 days, N=16), compared to matched control animals (N=21). T-tubule density, ryanodine receptor (RyR) distribution, and local [Ca(2+)](i) transients were examined in confocal imaging. RESULTS: Myocyte shortening and underlying [Ca(2+)](i) transients were profoundly reduced in AF (by 54.8% and 62%, P<0.01). This reduced cell shortening could be corrected by increasing [Ca(2+)](i). SR Ca(2+) content was not different. Calculated fractional SR Ca(2+) release was reduced in AF (by 20.6%, P<0.05). Peak Ca(2+) current density was modestly decreased (by 23.9%, P<0.01). T-tubules were present in the control atrial myocytes at low density and strongly reduced in AF (by 45%, P<0.01), whereas the regular distribution of RyR was unchanged. Synchrony of SR Ca(2+) release in AF was significantly reduced with increased areas of delayed Ca(2+) release. Propagation between RyR was unaffected but Ca(2+) release at subsarcolemmal sites was reduced. Rate of Ca(2+) extrusion by Na(+)/Ca(2+) exchanger was increased. CONCLUSIONS: In persistent AF, reduced SR Ca(2+) release despite preserved SR Ca(2+) content is a major factor in contractile dysfunction. Fewer Ca(2+) channel-RyR couplings and reduced efficiency of the coupling at subsarcolemmal sites, possibly related to increased Na(+)/Ca(2+) exchanger, underlie the reduction in Ca(2+) release.

Author information

Author/s: Lenaerts, Ilse (I); Bito, Virginie (V); Heinzel, Frank R (FR); Driesen, Ronald B (RB); Holemans, Patricia (P); D'hooge, Jan (J); Heidbüchel, Hein (H); Sipido, Karin R (KR); Willems, Rik (R);

Affiliation: Experimental Cardiology, KUL, Campus Gasthuisberg O/N 7th Floor, Herestraat 49, B-3000 Leuven, Belgium.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Circulation research (Circ Res), published in United States. (Language: eng)

Reference: 2009-Oct; vol 105 (issue 9) : pp 876-85

Dates: Created 2009/10/23; Completed 2009/11/05;

PMID: 19762679, status: MEDLINE (last retrieval date: 11/5/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals Atrial Fibrillation - metabolism; pathology; physiopathology Atrial Function, Right Calcium Channels, L-Type - metabolism Calcium Signaling Disease Models, Animal Electrophysiologic Techniques, Cardiac Female Glycogen - metabolism Heart Atria - metabolism; pathology; physiopathology

Membrane Potentials Microfilaments - metabolism Myocardial Contraction Myocytes, Cardiac - metabolism; ultrastructure Ryanodine Receptor Calcium Release Channel - metabolism Sarcolemma - metabolism Sarcoplasmic Reticulum - metabolism; ultrastructure Sheep Sodium-Calcium Exchanger - metabolism Time Factors

Associated Chemicals: Calcium Channels, L-Type (0) ; Ryanodine Receptor Calcium Release Channel (0) ; Sodium-Calcium Exchanger (0) ; Glycogen (9005-79-2)

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