Volume regulatory activity of the Ehrlich ascites tumor cell and its relationship to ion transport.
The volume regulatory response of the Ehrlich ascites tumor was studied in KCl-depleted, Na+-enriched cells. Subsequent incubation in K+-containing NaCl medium results in the reaccumulation of K+, Cl-, water and the extrusion of Na+. The establishment of the physiological steady state is due primarily to the activity of 2 transport systems. One is the Na/K pump (KM for K+o = 3.5 mM; Jmax = 30.1 mEq/kg dry min), which in these experiments was coupled 1K+/1 Na+. The second is the Cl--dependent (Na+ + K+) cotransport system (KM for K+o = 6.8 mM; Jmax = 20.8 mEq/kg dry min) which mediates, in addition to net ion uptake in the ratio of 1K+:1Na+:2Cl-, the exchange of K+i for K+o. The net passive driving force on the cotransport system is initially inwardly directed but does not decrease to zero at the steady state. This raises the possibility of the involvement of an additional source of energy. Although cell volume increases concomitant with net ion uptake, this change does not appear to be a major factor regulating the activity of the cotransport system.
Levinson
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Department of Physiology, University of Texas Health Science Center, San Antonio 78284-7756.
D000818:Animals; D002286:Carcinoma, Ehrlich Tumor / Q000473:pathology / Q000503:physiopathology*; D002712:Chlorides / Q000502:physiology*; D004058:Diffusion; D005665:Furosemide / Q000494:pharmacology; D007700:Kinetics; D051379:Mice; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000502:physiology*; D012964:Sodium / Q000502:physiology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology; D014407:Tumor Cells, Cultured / Q000502:physiology; D014882:Water-Electrolyte Balance / Q000187:drug effects
D002712:Chlorides; D010042:Ouabain; D005665:Furosemide; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium