Stimulation of flounder erythrocytes by noradrenaline under isosmotic conditions (330 mosmol kg-1) and physiological Na+ concentration (113 mmol l-1) caused swelling of the cells. The EC50 of this cell swelling was 0.65 µmol l-1 noradrenaline. The effect of the noradrenaline-induced cell swelling on the taurine channel under isosmotic conditions was negligible. However, when the cells were stimulated by noradrenaline (1.0 µmol l-1) before, simultaneously with or after reduction of osmolality (255 mosmol kg-1), the volume regulatory efflux of taurine mediated by the taurine channel was transiently accelerated. The rate coefficient for taurine efflux was more than four times higher than in osmolality-stimulated cells not exposed to noradrenaline. The present paper deals with the accelerating effect of noradrenaline on the taurine channel under hypo-osmotic conditions and the lack of effect of noradrenaline-induced cell swelling on the channel under iso-osmotic conditions. Noradrenaline initiated the cell swelling by interacting with ß-receptors which appeared to be more related to the mammalian ß1-receptors than to the ß2-receptors. The receptor interaction activated the adenylate cyclase system and, in the presence of 1.0 µmol l-1 noradrenaline, the cellular cyclic AMP concentration increased about 23 times. Noradrenaline also stimulated the Na+/H+ and Cl-/HCO3- antiporters and this affected the extracellular pH as well as the cell volume. Depending on the extracellular Na+ concentration, the incubation medium was acidified (113 mmol l-1 Na+) or alkalized (2.7 mmol l-1 Na+). Under these two conditions, the accelerating effects of noradrenaline on the taurine efflux were of similar magnitude. Similar effects on the cell volume, the extracellular pH and the volume regulatory taurine efflux were obtained in the presence of the cyclic AMP analogue 8-bromo-cyclic AMP. Under hypo-osmotic conditions in the absence of noradrenaline, the cellular level of cyclic AMP was not elevated. There was no significant positive correlation between the water content of the cells (cell volume) under different conditions in the presence or absence of noradrenaline and the state of activation of the osmolality-sensitive taurine channel. We conclude that the mechanism(s) which activate(s) the osmolality-sensitive taurine channel in flounder erythrocytes is transiently and strongly accelerated by noradrenaline, but not triggered by the noradrenaline-induced events. The acceleration does not appear to be due to increased activity of the antiporters, but to increased cellular levels of cyclic AMP.