Several reports have documented that thapsigargin is a potent inhibitor of the SR Ca2+ ATPase isolated from cardiac or skeletal muscle. We have characterized the specificity of this agent in intact rat cardiac myocytes using cells maintained in the whole cell voltage clamp configuration. We have shown that thapsigargin decreases the magnitude of the Ca2+ transient and the twitch by about 80% while it slows the decay rate for these responses. These changes were not accompanied by any alterations in sarcolemmal currents or in the trigger Ca2+ generated by the inward calcium current. Taken together these results reveal that the action of thapsigargin is restricted to the SR Ca2+ ATPase in intact cardiac myocytes. Furthermore, it is demonstrated unambiguously that SR intracellular Ca2+ stores are an absolute requirement for the development of contractile tension in rat heart myocytes. It is shown that thapsigargin is a valuable probe to examine the importance of SR pools of Ca2+ and the role of the Ca2+ ATPase in intact myocytes as well as in genetically altered heart cells.
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Review Article|
October 01 1995
Use of thapsigargin to study Ca2+ homeostasis in cardiac cells
Terry B. Rogers;
Terry B. Rogers
1Department of Biological Chemistry, University of Maryland School of Medicine, Baltimore, Maryland 21201
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Giuseppe Inesi;
Giuseppe Inesi
1Department of Biological Chemistry, University of Maryland School of Medicine, Baltimore, Maryland 21201
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Robert Wade;
Robert Wade
1Department of Biological Chemistry, University of Maryland School of Medicine, Baltimore, Maryland 21201
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W. J. Lederer
W. J. Lederer
2Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201
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Publisher: Portland Press Ltd
Received:
September 15 1995
Online ISSN: 1573-4935
Print ISSN: 0144-8463
© 1995 Plenum Publishing Corporation
1995
Biosci Rep (1995) 15 (5): 341–349.
Article history
Received:
September 15 1995
Citation
Terry B. Rogers, Giuseppe Inesi, Robert Wade, W. J. Lederer; Use of thapsigargin to study Ca2+ homeostasis in cardiac cells. Biosci Rep 1 October 1995; 15 (5): 341–349. doi: https://doi.org/10.1007/BF01788366
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