Journal article
Mitochondrial F1-ATPase activity of canine myocardium: effects of hypoxia and stimulation
The American journal of physiology, Vol.266(6 Pt 2), pp.H2396-H2403
06/1994
DOI: 10.1152/ajpheart.1994.266.6.h2396
PMID: 8024001
Abstract
Recent studies have suggested that modifications in mitochondrial F1-adenosinetriphosphatase (ATPase) activity may play an important role in the regulation of myocardial oxidative phosphorylation. The goal of the present study was to develop and characterize an assay of F1-ATPase activity that could be performed repeatedly on an intact heart under various physiological states. With the use of submitochondrial particles prepared from biopsy samples of canine myocardium, we found reproducible F1-ATPase activity when normalized to the activity of the intramitochondrial enzyme citrate synthase. The oligomycin-sensitive component of the ATPase activity was found to be mainly F1-ATPase. F1-ATPase activity of normal myocardium increased by incubation in high salt-pH buffer, suggesting baseline inhibition. Five minutes after global ischemia, F1-ATPase activity decreased to 60% of baseline. Hypoxia for 10 min resulted in no significant change in F1-ATPase activity. With phenylephrine infusion, myocardial oxygen consumption more than doubled, whereas F1-ATPase activity increased by approximately 30%. Both returned to baseline levels after discontinuation of the drug. With the use of an assay developed to measure F1-ATPase activity of intact myocardium, changes of the enzyme activity were found during both ischemia and at increased work loads. These data suggest that alterations of F1-ATPase activity may contribute to the regulation of myocardial oxidative phosphorylation.
Details
- Title: Subtitle
- Mitochondrial F1-ATPase activity of canine myocardium: effects of hypoxia and stimulation
- Creators
- Thomas D Scholz - National Heart Lung and Blood InstituteRobert S Balaban - National Heart Lung and Blood Institute
- Resource Type
- Journal article
- Publication Details
- The American journal of physiology, Vol.266(6 Pt 2), pp.H2396-H2403
- DOI
- 10.1152/ajpheart.1994.266.6.h2396
- PMID
- 8024001
- ISSN
- 0002-9513
- eISSN
- 2163-5773
- Language
- English
- Date published
- 06/1994
- Academic Unit
- Cardiology; Stead Family Department of Pediatrics; Fraternal Order of Eagles Diabetes Research Center; Child and Community Health
- Record Identifier
- 9984353842802771
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