© 2001 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
The importance of calcium in interpretation of NaK-ATPase isoform function in the mouse heart
Institute of Molecular Pharmacology and Biophysics, University of Cincinnati College of Medicine, 231 Bethesda Avenue, Cardiovascular Research Center, Cincinnati, OH 45267-0828, USA
* Corresponding author. Tel.: +1-513-5582-400; fax: +1-513-5581-778
Received 2 April 2001; accepted 23 April 2001
KEYWORDS Calcium (cellular); Na/K-pump
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We have recently emphasized an important role for intracellular calcium in changes that occur in the adrenergic system in cardiac hypertrophy and failure in the mouse heart [1,2]. For example, the blunting or loss of function of the β-adrenergic receptor signaling pathway that has been described for a number of mouse transgenic models can be restored to normal by "unloading" the heart of calcium [2]. It is well known that the isolated rat heart responds in a perfectly normal manner to a variety of pharmacological agents including digitalis and to physiological stimuli, but only when the perfusion media contains "low" calcium, ranging from 0.25 to 1.0 mM [3–7].
Less is known about the isolated mouse heart although most agree that the calcium requirements for pharmacological and physiological studies are the same as the rat [5].
In the case of the NaK-ATPase (NKA) three 
isoforms have been
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