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Effects of semi-starvation and potassium deficiency on the concentration of [3H]ouabain-binding sites and sodium and potassium contents in rat skeletal muscle

Published online by Cambridge University Press:  09 March 2007

Keld Kjeldsen ,
Maria Elisabeth Everts  and
Torben Clausen
Keld Kjeldsen
Affiliation:
Institute of Physiology, University of Aarhus, DK-8000 Aarhus C, Denmark
Maria Elisabeth Everts
Affiliation:
Institute of Physiology, University of Aarhus, DK-8000 Aarhus C, Denmark
Torben Clausen
Affiliation:
Institute of Physiology, University of Aarhus, DK-8000 Aarhus C, Denmark
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Abstract

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1. Using vanadate-facilitated [3H]ouabain binding, the effect of semi-starvation on the total concentration of [3H]ouabain-binding sites was determined in samples of rat skeletal muscle. When 12-week-old rats were semi-starved for 1, 2 or 3 weeks on one-third to half the normal daily energy intake, the [3H]ouabain-binding site concentration in soleus muscle was reduced by 19, 24 and 25% respectively. In extensor digitorum longus, diaphragm and gastrocnemius muscles the decrease after 2 weeks of semi-starvation was 15, 18 and 17% respectively. The decrease was fully reversible within 3 d of free access to the diet. Complete deprivation of food for 5 d caused a reduction of 25% in soleus muscle [3H]ouabain-binding-siteconcentration. It was excluded that the reduction in [3H]ouabain binding was due to a reduced affinity of the binding site for [3H]ouabain.

2. Semi-starvation of 12-week-old rats for 3 weeks caused a reduction of 45 and 53% in 3, 5, 3'-triiodothyronine (T3) and thyroxine (T4) levels respectively. As reduced thyroid hormone levels have previously been found to decrease [3H]ouabain-binding-siteconcentration in skeletal muscle, this points to the importance of T3 and T4 in the down-regulation of the [3H]ouabain-binding-siteconcentration in skeletal muscle with semi-starvation. Whereas potassium depletion caused a decrease in K content as well as in [3H]ouabain-binding-siteconcentration in skeletal muscles, semi-starvation caused only a tendency to a decrease in K content. Thus, K depletion is not a major cause of the reduction in [3H]ouabain-binding-siteconcentration with semi-starvation.

3. Due to its high concentration of Na, K pumps, skeletal muscle has a considerable capacity for clearing K from the plasma as well as for the binding of digitalis glycosides. Semi-starvation causes a severe reduction in the total skeletal muscle pool of Na, K pumps and may therefore be associated with impairment of K tolerance and increased digitalis toxicity.

Type
Papers of direct relevance to Clinical and Human Nutrition
Information
British Journal of Nutrition , Volume 56 , Issue 3 , November 1986 , pp. 519 - 532
Copyright
Copyright © The Nutrition Society 1986

References

REFERENCES

Alexis, S. D., Vilaire, G. & Young, V. R. (1971). Journal of Nutrition 101, 273–286.CrossRefGoogle Scholar
Asano, Y., Liberman, U. A. & Edelman, I. S. (1976). Journal of Clinical Investigation 57, 368–379.CrossRefGoogle Scholar
Biron, R., Burger, A., Chinet, A., Clausen, T. & Dubois-Ferriere, R. (1979). Journal of Physiology 297, 47–60.CrossRefGoogle Scholar
Brown, L., Wagner, G., Hug, E. & Erdmann, E. (1986). Cardiovascular Research (In the Press).Google Scholar
Burman, K. D., Lukes, Y., Wright, F. D. & Wartofsky, L. (1977). Endocrinology 101, 1331–1334.CrossRefGoogle Scholar
Clausen, T. (1986). Physiological Review 66, 542–580.CrossRefGoogle Scholar
Clausen, T. & Hansen, O. (1982). Biochemical and Biophysical Research Communications 104, 357–362.CrossRefGoogle Scholar
Clausen, T., Hansen, O., Kjeldsen, K. & Nørgaard, A. (1982). Journal of Physiology 333, 367–381.CrossRefGoogle Scholar
Clausen, T. & Kjeldsen, K. (1986). In Current Topics in Membranes and Transport. New York and London: Academic Press (In the Press).Google Scholar
Germain, D. L. S. & Galton, V. A. (1985). Journal of Clinical Investigation 75, 679–688.CrossRefGoogle Scholar
Hansen, O. & Skou, J. C. (1973). Biochimica et Biophysica Acta 311, 51–66.CrossRefGoogle Scholar
Hazeyama, Y. & Sparks, H. V. (1979). American Journal of Physiology 5, R83–R90.Google Scholar
Hermansen, L., Orheim, A. & Sejersted, O. M. (1984). International Journal of Sports Medicine 5, Suppl., 110–115.CrossRefGoogle Scholar
Hirche, H., Schumacher, E. & Hagemann, H. (1980). Pflügers Archiv 387, 231–237.CrossRefGoogle Scholar
Jones, L. R. & Besch, H. R. (1984). Methods in Pharmacology 5, 1–12.Google Scholar
Kjeldsen, K. (1986). Danish Medical Bulletin (In the Press).Google Scholar
Kjeldsen, K., Everts, M. E. & Clausen, T. (1986 a). Pflügers Archiv 406, 529–535.CrossRefGoogle Scholar
Kjeldsen, K., Nørgaard, A. & Clausen, T. (1984). Acta Physiologica Scandinavica 122, 103–117.CrossRefGoogle Scholar
Kjeldsen, K., Nørgaard, A., Hansen, O. & Clausen, T. (1985). Journal of Pharmacology and Experimental Therapeutics 234, 720–727.Google Scholar
Kjeldsen, K., Richter, E. A., Galbo, H., Lortie, G. & Clausen, T. (1986 b). Biochimica et Biophysica Acta (In the Press).Google Scholar
Knochel, J. P. (1982). American Journal of Medicine 72, 521–535.CrossRefGoogle Scholar
Knochel, J. P., Blachley, J. D., Johnson, J. H. & Carter, N. W. (1985). Journal of Clinical lnvestigafion 75, 740–745.CrossRefGoogle Scholar
Lin, M. H. & Akera, T. (1978). Journal of Biological Chemistry 253, 723–726.CrossRefGoogle Scholar
Lin, M. H., Romsos, D. R., Akera, T. & Leveille, G. A. (1978). Biochemical and Biophysical Research Communications 80, 398–404.CrossRefGoogle Scholar
Lindeman, R. D. & Pederson, J. A. (1983). In Potassium: its Biologic Significance, pp, 46–76 [Whang, R. and Aikawa, J. K., editors]. Boca Raton, Florida: CRC Press Inc.Google Scholar
Nørgaard, A., Kjeldsen, K. & Clausen, T. (1981). Nature 293, 739–741.CrossRefGoogle Scholar
Nørgaard, A., Kjeldsen, K. & Hansen, O. (1985). European Journal of Pharmacology 113, 373–382.CrossRefGoogle Scholar
Nørgaard, A., Kjeldsen, K., Hansen, O. & Clausen, T. (1983). Biochemical and Biophysical Research Communications 111, 319–325.CrossRefGoogle Scholar
Schussler, G. C. & Orlando, J. (1978). Science 199, 686–687.CrossRefGoogle Scholar
Swann, A. C. (1984). American Journal of Physiology 247, R449–R455.Google Scholar
Tibes, U., Hemmer, B., Böning, D. & Schweigart, U. (1976). European Journal of Applied Physiology 35, 201–214.CrossRefGoogle Scholar
Tibes, U., Hemmer, B., Schweigart, U., Böning, D. & Fotescu, D. (1974). Pflügers Archiv 347, 145–158.CrossRefGoogle Scholar
Vagenakis, A. G., Burger, A., Portnay, G. I., Rudolph, M., O'Brian, J. T., Azizi, F., Arky, R. A., Nicod, P., Ingbar, S. H. & Braverman, L. E. (1975). Journal of Clinical Endocrinology and Metabolism 41, 191–194.CrossRefGoogle Scholar