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D C TOSTESON

Publications and source records attributed to D C TOSTESON.

15 recordsLinked to original sources
PubMed1960

Regulation of cell volume by active cation transport in high and low potassium sheep red cells.

A model cell which controls its cation composition and volume by the action of a K-Na exchange pump and leaks for both ions working in parallel is presented. Equations are formulated which describe the behavior of this model in terms of three membrane parameters. From these equations and the steady state concentrations of Na, K, and Cl, values for these parameters in high potassium (HK) and low potassium (LK) sheep red cells are calculated. Kinetic experiments designed to measure the membrane parameters directly in the two types of sheep red cells are also reported. The values of the parameters obtained in these experiments agreed well with those calculated from the steady state concentrations of ions and the theoretical equations. It is concluded that both HK and LK sheep red cells control their cation composition and volume in a manner consistent with the model cell. Both have a cation pump which exchanges one sodium ion from inside the cell with one potassium ion from outside the cell but the pump is working approximately four times faster in the HK cell. The characteristics of the cation leak in the two cell types are also very different since the HK cells are relatively more leaky to sodium as compared with potassium than is the case in the LK cells. Both cell types show appreciable sodium exchange diffusion but this process is more rapid in the LK than in the HK cells.

Animals↗
PubMed1955

The effects of sickling on ion transport. I. Effect of sickling on potassium transport.

The conversion of red cells of patients with sickle cell anemia (S-S) from biconcave disk to sickle shape by removal of oxygen was found to increase the fraction of medium trapped in cells packed by centrifugation from 0.036 (S.E. 0.003) to 0.106 (S.E. 0.004). The fraction of water in the cells (corrected for trapped medium) was not affected by this shape transformation. Cation transport, however, was changed profoundly. S-S cells incubated in N(2) rather than O(2) showed net K loss with acceleration of both influx and outflux. That this change in K transport was due to the process of sickling was indicated by (1) the persistence of the effect in the absence of plasma, (2) the absence of the effect in hypoxic S-S cells in which sickling was inhibited by alkali or carbon monoxide, (3) the reversal of the effect when sickling was reversed by exposure to O(2), and (4) the independence of the effect from such potentially important factors as age of the cell population. The acceleration of K transport by sickling is probably mediated by modification of the cell surface rather than the cell interior since concentrated sickle hemoglobin solutions in O(2) or N(2) did not show selective affinity for K. In molecular terms, the effect of sickling on K transport can be explained by presuming that the shape change (1) opens pathways for the free diffusion of K, and (2) accelerates K transport by a non-diffusion carrier process. The evidence for the former mechanism included (a) dependence of K influx into sickled cells on the concentration of K in the medium, and (b) increase in the total cation content of sickled cells with increasing pH. Observations suggestive of a carrier process included (a) the failure of sickled cell K concentration to become equal to external K concentration even after 48 hours, (b) the deviation of the flux ratio from that characteristic of diffusion, and (c) the dependence of K influx on glycolysis.

Anemia, Sickle Cell↗
PubMed1955

The effects of sickling on ion transport. II. The effect of sickling on sodium and cesium transport.

When the red cells from patients with sickle cell anemia (S-S) were kept in the disk shape by incubation in O(2), they maintained cell sodium in the steady state for at least 10 hours. The sodium flux in such cells at 37 degrees C. was 6.0 +/- 1.5 m.eq./ (liters RBC) x (hours). When S-S cells were sickled by incubation in N(2), sodium outflux increased two- to threefold, while influx increased four- to fivefold and the cells gained net sodium. A small but undetermined fraction of the sodium in disk and sickle shaped S-S cells exchanges at one or more rates which are substantially slower than those calculated here from the initial rate of transfer of tracer from cells to the medium. The penetration of tracer Cs into normal and both disk and sickled S-S cells was markedly inhibited by increasing the K concentration in the medium, indicating that Cs and K compete for an entrance pathway in all three cell types. The ratio of the inward rate constant for tracer Cs to that for K(42) in normal and disk-shaped S-S cells increased only slightly when the K concentration in the medium was increased, indicating that almost all the Cs entered such cells in competition with K. Sickling accelerated the entrance of tracer cesium into S-S cells. Furthermore, the rate constant ratio increased with increasing external K concentration in sickled cells, suggesting the simultaneous presence of a non-competitive route for cesium influx in this cell type. The results are interpreted to support the view that sickling (a) accelerates inward transport of K and Cs and outward transport of Na by a non-diffusion, assumed carrier, process and (b) opens pathways for the diffusion of all three ions.

Anemia, Sickle Cell↗