Abstract
Cold-stored human erythrocytes exposed to an artificial buffer transport less potassium inward than do control cells exposed only to plasma. The deficit increases with the amount of exposure of the cells to the buffer. It is proposed that some easily-removed lipid component of the red cell membrane is necessary for maximal potassium transport by the erythrocyte. Exposure of cells to buffer does not alter their responses to ouabain or to inosine.
Calcium levels below normal have no effect on potassium influx into cells suspended in plasma or in buffer. Calcium levels higher than normal progressively decrease potassium influx into incubated cold-stored erythrocytes, whether the cells be suspended in plasma or in buffer. Neither strontium nor magnesium ions produced this effect. Inhibition produced by high levels of calcium is additive with that produced by ouabain.
Ca45 disappears from plasma exposed to fresh or cold-stored red cells. The disappearance can be accounted for by 3 processes: 1) a rapid distribution, probably onto the surface of fresh or cold-stored cells, which is complete in less than 2 minutes; 2) a slow steady loss, probably diffusion into fresh and cold-stored cells; and 3) a more rapid process which occurs only in incubated cold-stored cells. High concentrations of ouabain did not affect any of these processes.
Calcium ions may block the access of potassium (or sodium) ions to some lipid component of the cell which is important to monovalent cation transport.
Footnotes
- Received May 9, 1958.
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