Early Signals in Serum-Induced Increases in Ouabain-Sensitive Na+-K+ Pump Activity and in Glucose Transport in Rat Skeletal Muscle Are Amiloride-Sensitive
Article first published online: 5 OCT 2006
Journal of Neurochemistry
Volume 60, Issue 6, pages 2247–2253, June 1993
How to Cite
Brodie, C. and Sampson, S. R. (1993), Early Signals in Serum-Induced Increases in Ouabain-Sensitive Na+-K+ Pump Activity and in Glucose Transport in Rat Skeletal Muscle Are Amiloride-Sensitive. Journal of Neurochemistry, 60: 2247–2253. doi: 10.1111/j.1471-4159.1993.tb03511.x
- Issue published online: 5 OCT 2006
- Article first published online: 5 OCT 2006
- Received July 25, 1992; revised manuscript received October 10, 1992; accepted November 16, 1992.
- Na+-K+ pump;
- Na+-H+ exchange;
- Glucose transport;
- Membrane potential;
- Skeletal muscle.
Abstract: The acute effects of serum on sodium-potassium (Na+-K+) pump activity and glucose uptake in cultured rat skeletal muscle were studied. Addition of serum to myo-tubes in phosphate-buffered saline caused Na+-K+ pump activity (as measured by changes in the ouabain-sensitive component of both membrane potential and 86Rb uptake) to increase, with peak effects obtained after 30 min. The effect was blocked completely by treatment with amiloride, but not by tetrodotoxin, which blocks voltage-dependent Na+ channels. On transfer of myotubes to Na+-free, choline buffer, resting Na+-K+ pump activity decreased to about 10% of that in phosphate-buffered saline. Addition of regular serum, but not Na+-free serum, caused Na+-K+ pump activity to increase slightly. Similar results were obtained with serum on glucose uptake, the peak effect being reached within 15 min. Stimulation of glucose uptake by serum was partially reduced by amiloride and was not altered by tetrodotoxin. Removal of external Na+ also eliminated serum effects on glucose uptake. The results demonstrate that there are similar signals involving Na+-H+ exchange for serum-induced increases in Na+-K+ pump activity and glucose transport. The lack of complete blockade of serum-induced elevation of glucose transport suggests an additional, as yet undefined, intracellular signal for stimulation of this transport system.