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(Received for publication, July 1, 1996, and in revised form, September 4, 1996)
From the Department of Physiology and Biophysics, University of
Southern California School of Medicine,
Los Angeles, California 90033
During potassium deprivation, skeletal muscle
loses K+ to buffer the fall in extracellular
K+. Decreased active K+ uptake via the sodium
pump, Na,K-ATPase, contributes to the adjustment. Skeletal muscle
expresses
Volume 271, Number 51,
Issue of December 20, 1996
pp. 32653-32658
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
and 
Subunit Protein Levels
Respond to Hypokalemic Challenge with Isoform and Muscle Type
Specificity
1, 2, 
1, and 2 isoforms of the Na,K-ATPase
heterodimer. This study was directed at testing the hypothesis that
K+ loss from muscle during K+ deprivation is a
function of decreased expression of specific isoforms expressed in a
muscle type-specific pattern. Isoform abundance was measured in soleus,
red and white gastrocnemius, extensor digitorum longus, and diaphragm
by immunoblot. 2 expression was uniform across control muscles,
whereas 1 and 1 were twice as high in oxidative (soleus and
diaphragm) as in fast glycolytic (white gastrocnemius) muscles, and
2 expression was reciprocal: highest in white gastrocnemius and
barely detectable in soleus and diaphragm. Following 10 days of
potassium deprivation plasma K+ fell from 4.0 to 2.3 mM, and there were distinct responses in glycolytic
versus oxidative muscles. In glycolytic white gastrocnemius 2 and 2 fell 94 and 70%, respectively; in mixed red
gastrocnemius and extensor digitorum longus both fell 60%, and 1
fell 25%. In oxidative soleus and diaphragm 2 fell 55 and 30%,
respectively, with only minor changes in 1. Although decreases in
2 and 2 expression are much greater in glycolytic than oxidative
muscles during K+ deprivation, both types of muscle lose
tissue K+ to the same extent, a 20% decrease, suggesting
that multiple mechanisms are in place to regulate the release of
skeletal muscle cell K+.
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