Na+, Cl− cotransport in Ehrlich ascites tumor cells activated during volume regulation (regulatory volume increase)

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Abstract
Ehrlich ascites cells were preincubated in hypotonic medium with subsequent restoration of tonicity. After the initial osmotic shrinkage the cells recovered their volume within 5 min with an associated KCl uptake. 1. The volume recovery was inhibited when NO 3 − was substituted for Cl−, and when Na+ was replaced by K+, or by choline (at 5mm external K+). 2. The volume recovery was strongly inhibited by furosemide and bumetanide, but essentially unaffected by DIDS. 3. The net uptake of Cl− was much larger than the value predicted from the conductive Cl− permeability. The unidirectional36Cl flux, which was insensitive to bumetanide under steady-state conditions, was substantially increased during regulatory volume increase, and showed a large bumetanide-sensitive component. 4. During volume recovery the Cl− flux ratio (influx/efflux) for the bumetanide-sensitive component was estimated at 1.85, compatible with a coupled uptake of Na+ and Cl−, or with an uptake via a K+, Na+, 2Cl− cotransport system. The latter possibility is unlikely, however, because a net uptake of KCl was found even at low external K+, and because no K+ uptake was found in ouabain-poisoned cells. 5. In the presence of ouabain a bumetanide-sensitive uptake during volume recovery of Na+ and Cl− in nearly equimolar amounts was demonstrated. It is proposed that the primary process during the regulatory volume increase is an activation of an otherwise quiescent, bumetanide-sensitive Na+, Cl− cotransport system with subsequent replacement of Na+ by K+ via the Na+/K+ pump, stimulated by the Na+ influx through the Na+, Cl− cotransport system.

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