SUMMARY1. Swelling of trout erythrocytes can be induced either by addition of catecholamine to the cell suspension, thus promoting NaCl uptake via fiadrenergic-stimulated Na+-H+ exchange (isotonic swelling) or by suspending red blood cells in a hypotonic medium (hypotonic swelling). In both cases cells tend to regulate their volume by losing K+, but the characteristics of the volume-activated K+ pathways are different: after hormonally induced swelling the K+ loss is strictly Cl-dependent; after hypotonic swelling the K+ loss is essentially Cl-independent.2. In order to determine the nature of these volume regulatory pathways (i.e. whether the net K+ loss was conductive or was by electroneutral K+-H+ exchange or KCl co-transport), studies were performed to analyse ion fluxes and associated electrical phenomena. The cell membrane potential and intracellular ionic activities of volume-regulating and volume-static cells were measured by impalement with conventional microelectrodes and double-barrelled ion-sensitive microelectrodes.3. The information gained from the electrical and ion flux studies leads to the conclusion that both Cl--independent and Cl--dependent K+ loss proceed via electrically silent pathways.4. Experiments were designed to distinguish between electroneutral K+-H+ exchange or KCI co-transport. These were based upon the inhibition of Cl--OHexchange to evaluate the degree of coupling between K+ and Cl-(KCI stoichiometry, pH change). The experimental observations are consistent with the fact that both Cl--independent and Cl--dependent K+ loss are mediated by coupled K+-anion co-transport and not by K+-H+ exchange.5. On the basis of previous data, we suggest that only one type of K+-anion cotransport exists in the cell membrane, for which the selectivity for anions varies according to the change in cellular ionic strength induced by swelling.