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Am J Physiol Heart Circ Physiol 277: H74-H79, 1999;
0363-6135/99 $5.00
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Vol. 277, Issue 1, H74-H79, July 1999

Energy expenditure by Ba2+ contracture in rat ventricular slices derives from cross-bridge cycling

Hisaharu Kohzuki1, Hiromi Misawa1, Susumu Sakata1, Yoshimi Ohga1, Hiroyuki Suga2, and Miyako Takaki1

1 Department of Physiology II, Nara Medical University, Kashihara, Nara 634-852; and 2 Department of Physiology II, Okayama University Medical School, Okayama 700-8558, Japan

To clarify the energy-expenditure mechanism during Ba2+ contracture of mechanically unloaded rat left ventricular (LV) slices, we measured myocardial O2 consumption (VO2) of quiescent slices in Ca2+-free Tyrode solution and VO2 during Ba2+ contracture by substituting Ca2+ with Ba2+. We then investigated the effects of cyclopiazonic acid (CPA) and 2,3-butanedione monoxime (BDM) on the Ba2+ contracture VO2. The Ca2+-free VO2 corresponds to that of basal metabolism (2.32 ± 0.53 ml O2 · min-1 · 100 g LV-1). Ba2+ increased the VO2 in a dose-dependent manner (from 0.3 to 3.0 mmol/l) from 110 to 150% of basal metabolic VO2. Blockade of the sarcoplasmic reticulum (SR) Ca2+ pump by CPA (10 µmol/l) did not at all decrease the Ba2+-activated VO2. BDM (5 mmol/l), which specifically inhibits cross-bridge cycling, reduced the Ba2+activated VO2 almost to basal metabolic VO2. These energetic results revealed that the Ba2+-activated VO2 was used for the cross-bridge cycling but not for the Ca2+ handling by the SR Ca2+ pump.

oxygen consumption; excitation-contraction coupling; sarcoplasmic reticulum calcium adenosine 5'-triphosphatase; cyclopiazonic acid; 2,3-butanedione monoxime


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