Stimulation of bumetanide-sensitive K+ transport in Swiss 3T3 fibroblasts by serum and mitogenic hormones

✍ Scribed by Kurt Amsler; Jeremiah J. Donahue; Carolyn W. Slayman; Edward A. Adelberg

• Publisher: John Wiley and Sons
• Year: 1985
• Tongue: English
• Weight: 761 KB
• Volume: 123
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.1041230216

✦ Synopsis

Rapidly growing Swiss 3T3 fibroblasts possess a bumetanide-sensitive K + transport system that is dependent on both Na+ and CI-ions; a smaller bumetanide-insensitive component of K + transport is also present. In cells brought to the quiescent state by 8-11 days of incubation without a medium change, the bumetanide-sensitive rate of transport was reduced by 63%; the bumetanide-insensitive rate did not change. Removal of dialyzed fetal calf serum from the uptake medium resulted in a substantial reduction in bumetanide-sensitive uptake in both rapidly growing cells (33% reduction) and quiescent cells (68% reduction) but had no effect on bumetanide-insensitive uptake. Insulin was almost as effective as dialyzed fetal calf serum in stimulating bumetanide-sensitive uptake; insulin was maximally stimulatory at 2.5 Pgi ml. The combination of insulin, epidermal growth factor, and arginine-vasopressin was maximally effective in stimulating both bumetanide-sensitive K + uptake and 3H-thymidine incorporation in quiescent cells; bumetanide, however, did not interfere with the hormonal stimulation of DNA synthesis. Thus, the burnetanide-sensitive K + transport system is not necessary for such stimulation to occur. Furthermore, concentrations of hormones which stimulated significant levels of DNA synthesis produced no elevation in the intracellular concentration of K+. We conclude that the bumetanide-sensitive pathway of K + transport is modulated by serum and by mitogenic hormones, but does not play a role in the stimulation of DNA synthesis by these factors.