1. Sodium transport and intracellular sodium content were studied in thymocytes of rats made hypertensive by treatment for 4 or 8 weeks with deoxycorticosterone (DOC) and salt (DOC/salt). 2. The systolic blood pressure in the DOC/salt animals was 152 ± sem 3 and 189 ± 3 mmHg after 4 and 8 weeks' treatment respectively. This was significantly higher than pressures in their respective controls (124 ± 4 and 126 ± 5 mmHg), which had been given 1% sodium chloride solution (171 mmol/l) only. 3. The total sodium efflux rate constant in the DOC/salt rats was lower than that in the control group after 8 weeks of treatment (5.56 ± sem 0.21 vs 6.12 ± 0.11 h −1 ; P < 0.05) but not after 4 weeks of treatment (5.93 ± 0.13 vs 6.32 ± 0.13 h −1 ;0.1 > P > 0.05). 4. Intracellular sodium content in the DOC/salt rats was significantly higher than that of the control animals after 8 weeks' treatment (49.6 ± 2.5 vs 42.1 ± 1.0 mmol/kg dry weight; P < 0.05). 5. No significant changes were observed in intracellular potassium content, sodium influx or ouabain-insensitive sodium efflux rate constant.

1. The intracellular sodium content and the sodium efflux rate constant have been determined in vitro in thymocytes derived from the Okamato-Aoki strain of spontaneously hypertensive rats. 2. A strong positive correlation between the systolic blood pressure and the sodium content of thymocytes was observed ( r = 0.59, n = 39, P < 0.001). 3. The rate constant for total sodium efflux was negatively correlated with systolic blood pressure ( r = −0.43, n = 45, P < 0.005) and this was due to a fall in the ouabain-sensitive component of sodium efflux. 4. Sodium efflux, influx and the thymocyte potassium content were not related to the blood pressure.

1. The effect of extracellular potassium on the transport of sodium and potassium in rat thymocytes has been studied in vitro . 2. A significant increase in the rate constant for total and ouabain-sensitive sodium efflux was demonstrated at an extracellular potassium concentration of 1 mmol/l as compared with that at either 0 or 2 mmol/l. 3. At potassium concentrations below 3 mmol/l ouabain-sensitive sodium influx was observed suggesting sodium-sodium exchange catalysed by the sodium pump. 4. Both total and ouabain-insensitive potassium efflux rose with external potassium. A small ouabain-sensitive potassium efflux was observed at all levels of external potassium studied. 5. Total and ouabain-insensitive potassium influx increased with external potassium, but did not appear to saturate. Ouabain-sensitive potassium influx reached a maximum at an external potassium concentration of 2 mmol/l then decreased with increasing external potassium.

1. A significant correlation between leucocyte and muscle zinc contents was observed in control patients and in patients with generalized diseases. 2. As muscle contains a large proportion of the whole-body zinc, it is suggested that leucocyte zinc content may be a useful indicator of tissue zinc status.

1. The transport of zinc has been studied in normal human leucocytes incubated in both a tissue culture medium and Krebs buffer. 2. 65 Zn influx is characterized by an initial rapid phase followed by a slower influx. 65 Zn influx is directly dependent upon the extracellular zinc concentration. 3. Net zinc influx could only be demonstrated in Krebs buffer at zinc concentrations in excess of 4.3 μmol/l and in tissue culture fluid at zinc concentrations in excess of 43.1 μmol/l. 4. A 65 Zn efflux rate constant of approximately 1.0 per h was observed in both 4.3 and 15.4 μmol of zinc/l of Krebs buffer or tissue culture fluid. 5. In a zero external zinc Krebs buffer the 65 Zn efflux rate constant fell to 0.57 per h and was accompanied by a small net zinc efflux.

1. Leucocytes were isolated from blood of healthy volunteer subjects and incubated in media of which the bicarbonate, P co 2 and pH composition were varied. 2. The intracellular sodium, potassium and water content of leucocytes were virtually unaffected by the acid—base composition of the media used.