Does intracellular sodium modify membrane permeability to sodium ions?

Nature ◽  
1977 ◽  
Vol 266 (5601) ◽  
pp. 468-469 ◽  
Author(s):  
A. W. CUTHBERT ◽  
W. K. SHUM
1973 ◽  
Vol 61 (2) ◽  
pp. 222-250 ◽  
Author(s):  
R. A. Sjodin ◽  
L. A. Beaugé

Net sodium influx under K-free conditions was independent of the intracellular sodium ion concentration, [Na]i, and was increased by ouabain. Unidirectional sodium influx was the sum of a component independent of [Na]i and a component that increased linearly with increasing [Na]i. Net influx of sodium ions in K-free solutions varied with the external sodium ion concentration, [Na]o, and a steady-state balance of the sodium ion fluxes occurred at [Na]o = 40 mM. When solutions were K-free and contained 10-4 M ouabain, net sodium influx varied linearly with [Na]o and a steady state for the intracellular sodium was observed at [Na]o = 13 mM. The steady state observed in the presence of ouabain was the result of a pump-leak balance as the external sodium ion concentration with which the muscle sodium would be in equilibrium, under these conditions, was 0.11 mM. The rate constant for total potassium loss to K-free Ringer solution was independent of [Na]i but dependent on [Na]o. Replacing external NaCl with MgCl2 brought about reductions in net potassium efflux. Ouabain was without effect on net potassium efflux in K-free Ringer solution with [Na]o = 120 mM, but increased potassium efflux in a medium with NaCl replaced by MgCl2. When muscles were enriched with sodium ions, potassium efflux into K-free, Mg++-substituted Ringer solution fell to around 0.1 pmol/cm2·s and was increased 14-fold by addition of ouabain.


Life Sciences ◽  
1993 ◽  
Vol 52 (19) ◽  
pp. 1559-1565 ◽  
Author(s):  
J. Zicha ◽  
J. Kunes ◽  
K.H. Le Quan Sang ◽  
M.-A. Devynck

1968 ◽  
Vol 52 (3) ◽  
pp. 389-407 ◽  
Author(s):  
R. A. Sjodin ◽  
L. A. Beaugé

"Low sodium" muscles were prepared which contained around 5 mmoles/kg fiber of intracellular sodium. "High sodium" muscles containing between 15 and 30 mmoles/kg fiber of intracellular sodium were also prepared. In low sodium muscles application of 10-5 M strophanthidin reduced potassium influx by about 5%. Potassium efflux was unaffected by strophanthidin under these conditions. In high sodium muscles, 10-5 M strophanthidin reduced potassium influx by 45% and increased potassium efflux by 70%, on the average. In low sodium muscles sodium efflux was reduced by 25% during application of 10-5 M strophanthidin while in high sodium muscles similarly treated, sodium efflux was reduced by about 60%. Low sodium muscles showed a large reduction in sodium efflux when sodium ions in the Ringer solution were replaced by lithium ions. The average reduction in sodium efflux was 4.5-fold. Of the amount of sodium efflux remaining in lithium. Ringer's solution, 40% could be inhibited by application of 10-5 M strophanthidin. The total sodium efflux from low sodium muscles exposed to Ringer's solution in which lithium had been substituted for sodium ions for a period of 1 hr can be fractionated as 78% Na-for-Na interchange, 10% strophanthidin-sensitive sodium pump, and 12% residual sodium efflux. It is concluded that large strophanthidin-sensitive components of sodium and potassium flux can be expected only at elevated sodium concentrations within the muscle cells.


1981 ◽  
Vol 116 (1) ◽  
pp. 185-189 ◽  
Author(s):  
Luis CARRASCO ◽  
David VAZQUEZ ◽  
Carlos HERNANDEZ-LUCAS ◽  
Pilar CARBONERO ◽  
Francisco GARCIA-OLMEDO

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