KCl loss and cell shrinkage in the Ehrlich ascites tumor cell induced by hypotonic media, 2-deoxyglucose and propranolol.

Ehrlich ascites tumor cells lose KCl and shrink after swelling in hypotonic media and in response to the addition of 2-deoxyglucose, propranolol, or the Ca2+ ionophore, A23187, plus Ca2+ in isotonic media. All of these treatments activate cell shrinkage via a pathway with the following characteristics: (1) the KCl loss responsible for cell shrinkage does not alter the membrane potential; (2) NO3(-) does not substitute for Cl-; (3) the net KCl movements are not inhibited by quinine or DIDS; and (4) early in this study furosemide was effective in inhibiting cell shrinkage but this sensitivity was subsequently lost. This evidence suggests that the KCl loss in these cells occurs via a cotransport mechanism. In addition, hypotonic media and the other agents used here stimulate a Cl(-) - Cl(-) exchange, a net loss of K+ and a net gain of Na+ which are not responsible for cell shrinkage. The Ehrlich cell also appears to have a Ca2+-activated, quinine-sensitive K+ conductive pathway but this pathway is not part of the mechanism by which these cells regulate their volume following swelling or shrink in isotonic media in response to 2-deoxyglucose or propranolol. Shrinkage by the loss of K+ through the Ca2+ stimulated pathway appears to be limited by Cl- conductive movements; for when NO3(-), an anion demonstrated here to have a higher conductive movement than Cl-, is substituted for Cl-, the cells will shrink when the Ca2+-stimulated K+ pathway is activated.