544 E. HEINZ 
is usually assumed; these results seem to indicate that Nat ions support the glycine 
transport. They recall similar findings by CsAxy et al. with respect to the effect 
of Nat ions on the transport of sugars across the intestinal wall?’. 
As to the energetic coupling between glycine transport and K* exit, as suggested 
by Riccs ef al.'8, some of our observations do not support this hypothesis. Short- 
term reduction of cellular K* by preincubation with K*-free solutions, though greatly 
increasing K* influx, had no effect on glycine influx (Table II). The proposed me- 
chanism of this energetic coupling would also imply a strong competition between 
K+ and glycine inside the cell for the same carrier site. Hence increasing cellular 
glycine should depress K* efflux and favor K* accumulation. No such effect, however, 
has been found by KROMPHARDT AND GROBECKER in our laboratory!®, Similar 
findings have been reported by HEMPLING?®. We therefore assume that a relation- 
ship between the transport mechanisms for glycine and K*, if it exists, is not simply 
through an energetic coupling between K* exit and glycine entry. 
ACKNOWLEDGEMENT 
This work has been supported by a Grant (NSF-10812) of the National Science 
Foundation. 
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