HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Erlij, D Articles by Grinstein, S Search for Related Content PubMed PubMed Citation Articles by Erlij, D Articles by Grinstein, S

1. [3H]ouabain binding by frog sartorius muscles shows at least two components: one linked to inhibition of the pump and another not related to transport inhibition. This is suggested by the finding that [3H]ouabain uptake continued to increase when (a) the glycoside concentration was increased beyond that causing maximum transport inhibition, and (b) exposure times longer than those required to produce full inhibition were used. 2. A number of 1600 pumping sites per mum2 of membrane was estimated considering only the cylindrical surface of the muscle. 3. Insulin stimulated the ouabain-sensitive components of 22Na efflux and 134Cs influx. It also increased [3H]ouabain binding to a level of 1-7 times the total resting value. The increases in [3H]ouabain binding and in 22Na efflux followed a similar relationship with respect to insulin concentration. 4. Insulin stimulated the Na pump in muscles whose pumping sites had been inhibited by ouabain and then transferred to a glycoside-free solution. This stimulation was observed before detecting any recovery of the initial pumping activity. 5. When both the resting and the insulin-stimulated 22Na efflux had been blocked by ouabain, an additional dose of insulin, in a ouabain-free solution, had no further effects on 22Na efflux. 6. The effects of insulin were unaffected by cycloheximide or by high concentrations of butyryl derivatives of cyclic AMP and cyclic GMP. 7. We conclude that there are two pools of Na pumping sites in muscle cells: one active and another inactive. Insulin unmasks the inactive pumping sites by a mechanism that is independent of protein synthesis, increases in intracellular [Na] or decreases in intracellular [K].

This article has been cited by other articles:

				T. Clausen Regulatory role of translocation of Na+-K+ pumps in skeletal muscle: hypothesis or reality? Am J Physiol Endocrinol Metab, September 1, 2008; 295(3): E727 - E728. [Full Text] [PDF]

				A. V. Chibalin and B. Benziane Reply to Clausen letter Am J Physiol Endocrinol Metab, September 1, 2008; 295(3): E729 - E729. [Full Text] [PDF]

				B. Benziane and A. V. Chibalin Frontiers: Skeletal muscle sodium pump regulation: a translocation paradigm Am J Physiol Endocrinol Metab, September 1, 2008; 295(3): E553 - E558. [Abstract] [Full Text] [PDF]

				M. S. Rhee, A. Perianayagam, P. Chen, J. H. Youn, and A. A. McDonough Dexamethasone treatment causes resistance to insulin-stimulated cellular potassium uptake in the rat Am J Physiol Cell Physiol, November 1, 2004; 287(5): C1229 - C1237. [Abstract] [Full Text] [PDF]