The effects of potassium and membrane potential on sodium-dependent glutamic acid uptake.

The uptake of L-glutamic acid into brush-border membrane vesicles isolated from rat renal proximal tubules is NA+-dependent. In contrast to Na+-dependent uptake of D-glucose, pre-equilibration of the vesicles with K+ stimulates L-glutamic acid uptake. Imposition of a K+ gradient ([Ki+] > [Ko+]) further enhances Na+-dependent L-glutamic acid uptake, but leaves K+-dependent glucose transport unchanged. If K+ is present only at the outside of the vesicles, transport is inhibited. Intravesicular Rb+ and, to a lesser extent, Cs+ can replace intravesicular K+ to stimulate L-glutamic acid uptake. Changes in membrane potential incurred by the imposition of an H+-diffusion potential or anion replacement markedly affect Na+-dependent glutamic acid uptake only in the presence of K+. Experiments with a potential-sensitive cyanine dye also indicate that, in the presence of intravesicular K+ a charge movement is involved in Na+-dependent transport of L-glutamic acid. The data indicate that Na+-dependent L-glutamic acid transport can be additionally energized by a K+ gradient. Furthermore, intravesicular K+ render Na+-dependent L-glutamic acid transport sensitive to changes in the transmembrane electrical potential difference.