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.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002462:Cell Membrane / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism; D005971:Glutamates / Q000378:metabolism*; D066298:In Vitro Techniques; D007687:Kidney Tubules, Proximal / Q000378:metabolism / Q000502:physiology; D008297:Male; D008564:Membrane Potentials; D008871:Microvilli / Q000378:metabolism* / Q000502:physiology; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D012964:Sodium / Q000378:metabolism*
D005971:Glutamates; D012964:Sodium; D005947:Glucose; D011188:Potassium