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Department of Physiology and Biophysics, University of Southern California School of Medicine, Los Angeles, California 90033
When K+ output exceeds
input, skeletal muscle releases intracellular fluid
K+ to buffer the fall in
extracellular fluid (ECF) K+. To
investigate the mechanisms and muscle specificity of the K+ shift, rats were fed
K+-deficient chow for 2-10
days, and two muscles at phenotypic extremes were studied: slow-twitch
oxidative soleus and fast-twitch glycolytic white gastrocnemius
(WG). After 2 days of
low-K+ chow, plasma
K+ concentration
([K+]) fell from 4.6 to 3.7 mM, and
Na+-K+-ATPase
2 (not
1) protein levels in both muscles, measured by immunoblotting, decreased 36%. Cell
[K+] decreased from
116 to 106 mM in soleus and insignificantly in WG, indicating that
2
can decrease before cell
[K+].
After 5 days, there were further decreases in
2 (70%) and
2
(22%) in WG, not in soleus, whereas cell
[K+] decreased and
cell [Na+] increased
by 10 mM in both muscles. By 10 days, plasma
[K+] fell
to 2.9 mM, with further decreases in WG
2 (94%) and
2 (70%);
cell [K+] fell 19 mM
in soleus and 24 mM in WG compared with the control, and cell
[Na+] increased 9 mM
in soleus and 15 mM in WG; total homogenate
Na+-K+-ATPase
activity decreased 19% in WG and insignificantly in soleus. Levels of
2,
1, and
2 mRNA were unchanged over 10 days. The ratios of
2 to
1 protein levels in both control muscles were found to be
nearly 1 by using the relative changes in
-isoforms vs.
1-
(soleus) or
2-isoforms (WG). We conclude that the patterns of
regulation of Na+ pump isoforms in
oxidative and glycolytic muscles during
K+ deprivation mediated by
posttranscriptional regulation of
2
1 and
2
2 are distinct
and that decreases in
2-isoform pools can occur early enough in both
muscles to account for the shift of K+ to the ECF.
sodium-potassium-ATPase isoforms; hypokalemia; soleus; white gastrocnemius
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