1. The methods employed in these and preceding (25–27) studies were shown to allow analysis of true cellular sodium and potassium concentrations.
2. The rate of reaccumulation of potassium by potassium-deficient cells is independent of the presence or absence of sodium in the external medium.
3. Phenylurethane (10–3 M), a photosynthetic and metabolic inhibitor, causes a marked progressive loss of potassium and gain of sodium, both of which changes are completely reversible on transferring the samples to running sea water.
4. Iodoacetate, while not effective in causing potassium and sodium shifts in the light, effects a loss of potassium and a gain of sodium in the light in the presence of phenylurethane.
5. Arsenate (5 x 10–3 M) completely protects Ulva against the potassium loss usually observed with iodoacetate in the dark while it affords no protection against the sodium influx under the same conditions. Arsenate given after 18 to 20 hours in iodoacetate gives significant protection against potassium loss in the dark, and allows a slight net reaccumulation of potassium in the light. Arsenate in the dark after iodoacetate affords no protection against the sodium uptake caused by iodoacetate in the dark, while in the light under the same conditions sodium is rapidly secreted to the control level within a few hours. This resecretion of sodium is thought to be primarily an effect of light, the presence of arsenate being incidental.
6. The "decoupling agent" 4,6-dinitro-o-cresol causes a marked progressive increase in cellular sodium and a drop in cellular potassium, though the kinetics of these two movements are distinctly different from each other.
7. Pyruvate (50 mg. per cent) given with iodoacetate (2 x 10–3 M) for 5 hours in the dark completely prevents the sodium increase caused by iodoacetate, while affording less protection against the potassium loss. Phosphoglycerate, on the other hand, offers more protection against potassium loss, and essentially none against the sodium gain.
8. ATP added in small amounts at short intervals to samples maintained in 10–3 M iodoacetate in the dark affords significant protection against the potassium loss observed in iodoacetate. Cellular sodium is somewhat higher in the ATP-iodoacetate samples than in the iodoacetate samples.
9. In the discussion of the data presented two major points are emphasized: (1) the close correlation between cellular metabolism and normal cation control; (2) two mechanisms must be operative in cation regulation in this organism: one for moving potassium inwards and the other for transporting sodium outwards. These mechanisms are independent of each other.