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Regulation of the sodium‐potassium pump in cultured rat skeletal myotubes by intracellular sodium ions
Author(s) -
Brodie Chaya,
Sampson S. R.
Publication year - 1989
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041400116
Subject(s) - veratridine , ouabain , depolarization , sodium , chemistry , tetrodotoxin , biophysics , potassium , intracellular , diaphragm pump , membrane potential , myogenesis , skeletal muscle , biochemistry , medicine , endocrinology , sodium channel , biology , in vitro , materials science , organic chemistry , micropump , nanotechnology
The properties of the Na‐K pump and some of the factors controlling its amount and function were studied in rat myotubes in culture. The number of Na‐K pump sites was quantified by measuring the amount of [ 3 H]ouabain bound to whole‐cell preparations. Activity of the pump was determined by measurement of oua‐bain‐sensitive 86 Rb‐uptake and component of membrane potential. Chronic treatment of myotubes with tetrodotoxin (TTX), which lowers [Na]i, decreased the number of Na‐K pumps, the ouabain‐sensitive 86 Rb uptake, and the size of the electrogenic pump component of Em. In contrast, chronic treatment with either ouabain or veratridine, which increases [Na + ]i, resulted in an elevated level of Na‐K pump sites. This effect was blocked by inhibitors of protein synthesis. Neither rates of degradation nor affinity of pump sites in cells treated with TTX, veratridine, or ouabain differred from those in control cells. The number and activity of Na‐K pump sites were unaffected by chronic elevation in [Ca]i or chronic depolarization. We conclude that alterations in the level in intracellular Na ions play the major role in regulation of Na‐K pump synthesis in cultured mammalian skeletal muscle.