Energy expenditure by Ba(2+) contracture in rat ventricular slices derives from cross-bridge cycling.
To clarify the energy-expenditure mechanism during Ba(2+) contracture of mechanically unloaded rat left ventricular (LV) slices, we measured myocardial O(2) consumption (VO(2)) of quiescent slices in Ca(2+)-free Tyrode solution and VO(2) during Ba(2+) contracture by substituting Ca(2+) with Ba(2+). We then investigated the effects of cyclopiazonic acid (CPA) and 2,3-butanedione monoxime (BDM) on the Ba(2+) contracture VO(2). The Ca(2+)-free VO(2) corresponds to that of basal metabolism (2.32 +/- 0.53 ml O(2). min(-1). 100 g LV(-1)). Ba(2+) increased the VO(2) in a dose-dependent manner (from 0.3 to 3.0 mmol/l) from 110 to 150% of basal metabolic VO(2). Blockade of the sarcoplasmic reticulum (SR) Ca(2+) pump by CPA (10 micromol/l) did not at all decrease the Ba(2+)-activated VO(2). BDM (5 mmol/l), which specifically inhibits cross-bridge cycling, reduced the Ba(2+)activated VO(2) almost to basal metabolic VO(2). These energetic results revealed that the Ba(2+)-activated VO(2) was used for the cross-bridge cycling but not for the Ca(2+) handling by the SR Ca(2+) pump.
Department of Physiology II, Nara Medical University, Kashihara, Nara 634-852, Japan. hkohzuki@naramed-u.ac.jp
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Kohzuki
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Misawa
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Sakata
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Ohga
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Suga
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Takaki
D000818:Animals; D001464:Barium / Q000378:metabolism*; D002118:Calcium; D000252:Calcium-Transporting ATPases / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology*; D066298:In Vitro Techniques; D007211:Indoles / Q000494:pharmacology; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D010101:Oxygen Consumption; D051381:Rats; D017208:Rats, Wistar; D012519:Sarcoplasmic Reticulum / Q000502:physiology*; D016276:Ventricular Function
D007211:Indoles; D001464:Barium; D000252:Calcium-Transporting ATPases; D002118:Calcium; C000543:cyclopiazonic acid