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

  • Lenaerts I
  • Bito V
  • Heinzel F
 et al. 
  • 47

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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

Author-supplied keywords

  • *Atrial Function, Right
  • *Myocardial Contraction
  • Actin Cytoskeleton/metabolism
  • Animals
  • Atrial Fibrillation/*metabolism/pathology/physiopa
  • Calcium Channels, L-Type/metabolism
  • Calcium Signaling
  • Disease Models, Animal
  • Electrophysiologic Techniques, Cardiac
  • Female
  • Glycogen/metabolism
  • Heart Atria/metabolism/pathology/physiopathology
  • Membrane Potentials
  • Myocytes, Cardiac/*metabolism/*ultrastructure
  • Ryanodine Receptor Calcium Release Channel/metabol
  • Sarcolemma/*metabolism
  • Sarcoplasmic Reticulum/*metabolism/ultrastructure
  • Sheep
  • Sodium-Calcium Exchanger/metabolism
  • Time Factors

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Authors

  • I Lenaerts

  • V Bito

  • F R Heinzel

  • R B Driesen

  • P Holemans

  • J D'Hooge

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