Sodium and potassium transport in ferret red cells.

Potassium movements into ferret red cells were measured with the tracer 86Rb. Equilibration of 86Rb between medium and cells could be resolved into two components. 70‐90% occurred rapidly with a rate constant of between 3.5‐5.5 h‐1. The remaining 10‐30% occurred slowly. The slow movement was equivalent to a potassium influx of about 1.2‐2.76 mmol l‐1 cell h‐1. Potassium influx was inhibited by 80‐90% by 0.1 mM‐bumetanide (a high‐ceiling, loop diuretic). This suggests that the sodium‐potassium co‐transport system has a high capacity for carrying potassium (estimated at about 17‐35 mmol l‐1 cell h‐1). After bumetanide (0.1 mM) remaining potassium movements (approximately 0.5 mmol l‐1 cell h‐1) are at a similar level to that found in red cells from other animals. The sodium pump makes a very small contribution to potassium flux into ferret red cells. Much of this pump activity may be attributed to reticulocytes present in cell samples. Sodium movements across the red cell membrane were measured with 22Na. Sodium equilibrated more slowly than potassium. 60‐70% of the sodium influx was inhibited by 0.1 mM‐bumetanide, indicating that most sodium influx in ferret red cells is also through the co‐transport system. The co‐transport system can transport up to 49 mmol sodium l‐1 cell h‐1 and is half maximally activated by 0.38 mM‐potassium in the external medium. In the presence of bumetanide, sodium influx (about 18 mmol l‐1 cell h‐1) is similar to that of other carnivore red cells. This is about five times greater than that of red cells from non‐carnivores. The possibility that there are two populations of ferret red cells with different potassium transport characteristics is discussed.