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Am J Physiol Heart Circ Physiol 282: H1311-H1319, 2002. First published December 6, 2001; doi:10.1152/ajpheart.00464.2001
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Vol. 282, Issue 4, H1311-H1319, April 2002

Phase I and phase II of short-term mechanical restitution in perfused rat left ventricles

Cristian Dumitrescu1, Prakash Narayan1, Yuanna Cheng2, Igor R. Efimov2, and Ruth A. Altschuld1

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, Ohio 44195

We examined the contributions of the Ca2+ channels of the sarcolemma and of the sarcoplasmic reticulum to electromechanical restitution. Extrasystoles (F1) were interpolated 40-600 ms following a steady-state beat (F0) in perfused rat ventricles paced at 2 or 3 Hz. Plots of F1/F0 versus the extrasystolic interval consisted of phase I, which occurred before relaxation of the steady-state beat, and phase II, which occurred later. Phase I exhibited a period of enhanced left ventricular pressure development that coincided with action potential prolongation. Phase I was eliminated by -BAY K 8644 (100 nM) and FPL 64176 (150 nM), augmented by 3 µM thapsigargin plus 200 nM ryanodine and unaffected by KN-93 and KB-R7943. Phase II was accelerated by the Ca2+ channel agonists and by isoproterenol but was eliminated by thapsigargin plus ryanodine. The results suggest that phase I of electromechanical restitution is caused by a transient L-type Ca2+ current facilitation, whereas phase II represents the recovery of the ability of the sarcoplasmic reticulum to release Ca2+.

L-type calcium channels; sarcoplasmic reticulum; ryanodine receptors; myocardium; calmodulin


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