AJP - Heart Track the topics, authors and articles important to you
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 259: H1851-H1859, 1990;
0363-6135/90 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Doeller, J. E.
Right arrow Articles by Wittenberg, B. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Doeller, J. E.
Right arrow Articles by Wittenberg, B. A.

AJP - Heart and Circulatory Physiology, Vol 259, Issue 6 1851-H1859, Copyright © 1990 by American Physiological Society


ARTICLES

Intracellular calcium and high-energy phosphates in isolated cardiac myocytes

J. E. Doeller and B. A. Wittenberg
Department of Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, New York 10461.

The relationship between intracellular calcium (Cai) and high-energy phosphates was studied in adult cardiac myocytes. Cai and high-energy phosphates were measured in the same population of cells. Cai, reported by the fluorescence of fura-2, was maintained at normal levels in the presence of increased transsarcolemmal calcium gradients, up to 5 mM extracellular calcium concentration. Cai was experimentally elevated by increasing calcium influx from the extracellular medium and/or by diminishing calcium efflux by Na-Ca exchange. Under these conditions, cells contracted and relengthened repetitively. The regulation of high-energy phosphates was challenged by increasing ATP utilization and by inhibiting ATP synthesis. Cai regulation was not affected by inhibition of glycolysis or NADH oxidation, so long as ATP concentration remained unchanged. High-energy phosphates were not depleted in beating cells with intact NADH oxidation, but inhibition of NADH oxidation caused a significant drop in phosphocreatine, demonstrating the increased rate of ATP consumption during beating. In beating cells, as in the working heart, ATP supply is increased to meet ATP demand, and steady-state ATP and phosphocreatine concentrations remain unchanged.


This article has been cited by other articles:


Home page
Am. J. Physiol. Cell Physiol.Home page
F. Naro, V. De Arcangelis, D. Coletti, M. Molinaro, B. Zani, S. Vassanelli, C. Reggiani, A. Teti, and S. Adamo
Increase in cytosolic Ca2+ induced by elevation of extracellular Ca2+ in skeletal myogenic cells
Am J Physiol Cell Physiol, April 1, 2003; 284(4): C969 - C976.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
P. R. Territo, V. K. Mootha, S. A. French, and R. S. Balaban
Ca2+ activation of heart mitochondrial oxidative phosphorylation: role of the F0/F1-ATPase
Am J Physiol Cell Physiol, February 1, 2000; 278(2): C423 - C435.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
P. R. Territo, S. A. French, M. C. Dunleavy, F. J. Evans, and R. S. Balaban
Calcium Activation of Heart Mitochondrial Oxidative Phosphorylation. RAPID KINETICS OF mVO2, NADH, AND LIGHT SCATTERING
J. Biol. Chem., January 19, 2001; 276(4): 2586 - 2599.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online