The contribution of membrane transport to regulation of cytoplasmic pH in Chara corallina has been measured during proton-loading by uptake of butyric acid. In the short-term (i.e. up to 20 min) uptake of butyric acid is not affected by removal of external K+, Na+ or Cl− but over longer periods uptake is decreased (by 20–50% in different experiments) in the absence of external Na+ or, sometimes, K+. Influxes of both Na+ and K+ increase temporarily after addition of butyrate, Na+ immediately and K+ after a lag. Effects on Cl− influx are small but Cl− efflux increases enormously after a short lag. An approximate comparison of internal butyrate with changes in the concentration of K+, Na+, and Cl− suggests that initially (i.e. for a few min) cytoplasmic pH is determined by buffering and possibly by some decarboxylation of organic acids (biochemical pH regulation), and that biophysical pH regulation involving efflux of H+ balanced by influxes of K+, Na+ and especially efflux of Cl− progressively becomes dominant. When butyric acid is washed out of the cells, cytoplasmic pH is restored completely or partially (depending on the butyrate concentration used) and this is independent of the presence or absence of external Cl−. Where Cl− is present, its influx is relatively small. It is suggested that cytoplasmic pH is then controlled biochemically, involving the synthesis of an (unidentified) organic acid and the accumulation of acidic anions in place of butyurate lost from the cell. During the second application of butyrate, net Cl− efflux is small: it is suggested that control of cytoplasmic pH then involves decarboxylation of the organic acid anions. The questions of the source of Cl− lost from the cell (cytoplasm or vacuole) and of possible cytoplasmic swelling associated with the accumulation of butyrate are discussed.