I. Dorup, EFFECTS OF K-STEROIDS ON NA+, K+-PUMP CONCENTRATION IN SKELETAL-MUSCLE(, MG2+ DEFICIENCY AND ADRENAL), Acta Physiologica Scandinavica, 156(3), 1996, pp. 305-311
Animal studies have shown that deficiency of K+ is associated with a r
eduction in the concentration of Na+, K+ pumps in skeletal muscle, and
that this reduction is closely correlated with the reduction in the m
uscle K+ concentration. Furthermore. animals deficient in Mg+ show a d
ownregulation oi the Na+, K+-pump concentration. but this seems to be
secondary to the concomitant K+ deficiency. which often accompanies Mg
2+ deficiency. Measurements on skeletal muscle biopsies from patients
who had been in long-term treatment with diuretics showed that 55% had
reduced concentrations of both K+ and Mg2+, and that this was associa
ted with a reduction in the concentration of Na+, K+ pumps. Furthermor
e. the Na+, K+-pump concentration correlated significantly with both m
uscle K+ and Mg2+, suggesting that the downregulation of the Na+, K+ p
umps was related to the loss of K+, as predicted from the animal exper
iments. In accordance with this. normalization of muscle K+ and Mg2+ i
n response to oral Mg2+ supplementation. resulted in a restoration of
the Na+, K+ pumps. Apart from thyroid hormone, which is another major
regulator for the Na+, K+-pump concentration. other hormones may be of
importance. It is well known that adrenal steroids control the synthe
sis of Na+, K+ pumps in the kidney and heart. Recently. treatment with
dexamethasone was found to increase the Na+, K+-pump concentration in
rat skeletal muscle. The increase was found in EDL. soleus. gastrocne
mius and diaphragm muscles. and amounted to 23-52%. in contrast. treat
ment with aldosterone induced a decrease in the Na+, K+-pump concentra
tion. which was closely correlated to the reduced K+ content of the mu
scles. The results indicate that in skeletal muscle. high doses of glu
cocorticoids upregulate the concentration of Na+, K+ pumps, whereas mi
neralocorticoids induce a downregulation which is secondary to the con
comitant K+ deficiency.