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1 The Ohio State University Biophysics Program and Dorothy M. Davis Heart and Lung Research Institute, Columbus 43210; 2 The Cleveland Clinic Foundation, Department of Cardiology, Cleveland 44195; 3 Department of Food Science and Technology and 4 Department of Veterinary Biosciences, The Ohio State University, Columbus, Ohio 43210
We examined mechanical alternans and
electromechanical restitution in normal and failing rat hearts.
Alternans occurred at 5 Hz in failing versus 9 Hz in control hearts and
was reversed by 300 nM isoproterenol, 6 mM extracellular
Ca2+, 300 nM 
BAY K 8644, or 50 nM ryanodine. Restitution
curves comprised phase I, which was completed before relaxation of the
steady-state beat, and phase II, which occurred later. Phase I action
potential area and developed pressure ratios were significantly reduced in the failing versus control hearts. Phase II was a monoexponential increase in relative developed pressure as the extrasystolic interval was increased. The plateau of phase II was significantly elevated in
failing hearts. Thapsigargin (3 µM) plus ryanodine (200 nM) potentiated phase I to a significantly greater extent in control versus
failing hearts and abolished phase II in both groups. The results
suggest that both regulation of Ca2+ influx across the
sarcolemma and Ca2+ release by the sarcoplasmic reticulum
may contribute to altered excitation-contraction coupling in the
failing spontaneously hypertensive heart failure prone rat heart.
heart failure; calmodulin; sarcoplasmic reticulum; calcium current facilitation
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