Potassium migration and amino acid transport.

This communication undertakes to clarify a complex association between potassium distribution and amino acid transport. The transfer of amino acids into cells occurs best over a rather narrow range of extracellular potassium ion concentration (l-4). Furthermore, the uptake of neutral amino acids provokes a somewhat less than stoichiometric loss of potassium from the cells, with sodium ion replacement; the accumulated amino acids are in turn displaced when the extracellular potassium level is again elevated. This relationship is so much like that between two amino acids, each being displaceable by the other, that one cannot escape the thought that the potassium ion is behaving like an amino acid (2). In addition, a number of agents that stimulate amino acid accumulation also stimulate Kf loss from the cells, although, to confuse matters, this Kf loss becomes more conspicuous at higher levels of some of these agents where amino acid uptake is inhibited instead (5). The present study began with a finding, briefly reported (4), that glycine accumulation by the Ehrlich mouse ascitcs carcinoma cells falls off precipitously when the extracellular K+ level is kept well below the normal range. Further examination shows, however, that the transfer is depcndcnt instead upon the cellular potassium reservoir, the extracellula~ potassium serving to maintain cellular levels. In addition, K+ has been found necessary for the enhancement of amino acid uptake by pyridoxal.