Chloride accumulation in freshly isolated Ehrlich ascites tumor cells: the role of the Na/K/2Cl cotransporter.
When Ehrlich ascites tumor cells are removed from the peritoneal cavity and incubated in a saline solution, cells lose water, sodium, lactate and hydrogen ions and gain chloride. The gain of intracellular chloride exceeds that predicted from passive distribution. As chloride has been purported to play a role in volume regulation, it was of interest to identify factors responsible for controlling or maintaining intracellular chloride out of electrochemical equilibrium in Ehrlich cells. The results demonstrate that chloride accumulation in freshly isolated Ehrlich cells is sensitive to bumetanide, low extracellular K+ and low extracellular Na+, and is insensitive to DIDS. We conclude that chloride accumulation occurs due to the activity of the Na/K/2Cl cotransporter.
Thomas-Young
R J
RJ
Department of Physiology, University of Texas Health Science Center, San Antonio 78284-7756, USA.
Levinson
C
C
D000818:Animals; D002034:Bumetanide / Q000494:pharmacology; D002286:Carcinoma, Ehrlich Tumor / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002352:Carrier Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D002712:Chlorides / Q000378:metabolism*; D008297:Male; D008564:Membrane Potentials; D051379:Mice; D028021:Sodium-Potassium-Chloride Symporters; D014407:Tumor Cells, Cultured
D002352:Carrier Proteins; D002712:Chlorides; D028021:Sodium-Potassium-Chloride Symporters; D002034:Bumetanide