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Optical Mapping of Intra-Sarcoplasmic Reticulum Ca2+ and Transmembrane Potential in the Langendorff-perfused Rabbit Heart
09:26

Optical Mapping of Intra-Sarcoplasmic Reticulum Ca2+ and Transmembrane Potential in the Langendorff-perfused Rabbit Heart

Published on: September 10, 2015

Decreased sarcoplasmic reticulum calcium content is responsible for defective excitation-contraction coupling in

I A Hobai1, B O'Rourke

  • 1Institute of Molecular Cardiobiology, Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Md, USA.

Circulation
|March 21, 2001
PubMed

Insights

Reduced sarcoplasmic reticulum calcium (Ca(SR)) content, not altered excitation-contraction coupling, explains diminished intracellular calcium transients in heart failure. Therapeutics targeting Ca(SR) may restore normal calcium handling.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Physiology

Background:

  • Heart failure involves altered excitation-contraction (E-C) coupling, with decreased sarcoplasmic reticulum (SR) Ca uptake and enhanced Na/Ca exchange.
  • This may lead to reduced SR Ca content (Ca(SR)) and intracellular Ca (Ca(i)) transients.
  • Previous studies suggest reduced E-C coupling in other failure models, independent of SR Ca load.

Purpose of the Study:

  • Investigate alterations in Ca(SR) and E-C coupling in midmyocardial myocytes from failing canine hearts.
  • Determine if reduced Ca(SR) or impaired coupling underlies diminished Ca(i) transients in heart failure.

Main Methods:

  • Utilized indo-1-loaded myocytes from normal and failing canine hearts.
  • Measured Ca(i) transients using voltage-clamp steps at various frequencies.
  • Quantified Ca(SR) via Na/Ca exchange currents during caffeine-induced release.

Main Results:

  • Failing myocytes exhibited reduced Ca(i) transients (20-40% of normal) despite normal L-type Ca current (I(Ca,L)) density.
  • Ca(SR) was profoundly decreased in failing myocytes (15-25% of normal).
  • Restoring Ca(SR) in failing myocytes normalized the Ca(i) transient amplitude, indicating unaltered E-C coupling gain.

Conclusions:

  • A significant decrease in Ca(SR) is the primary cause of diminished Ca(i) transients in this heart failure model.
  • The intrinsic effectiveness of E-C coupling remains unchanged.
  • Therapies aimed at increasing Ca(SR) hold potential for correcting calcium handling deficits in heart failure.
Abstract

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