Stimulation of the efflux of L-glutamate from renal brush-border membrane vesicles by extravesicular potassium.
The rate of efflux of L-glutamate from renal brush-border membrane vesicles was enhanced by Na+ and by extravesicular L-glutamate, but not by D-glutamate nor analogs of L-glutamate that do not share the Na+-L-glutamate co-transport system. These results suggest that efflux was mediated by the Na+-L-glutamate carrier. The efflux of L-glutamate was increased by extravesicular K+ or Rb+ but not by Li+, choline+, or Tris+. These findings, together with previous results showing that intravesicular K+ or Rb+ increased L-glutamate uptake and that a K+ gradient energized the concentrative uptake of the acidic amino acid in the absence of other gradients, provide evidence consistent with the hypothesis that the co-transport of Na+-L-glutamate is coupled to the transmembrane flux of K+.
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D007668:Kidney / Q000378:metabolism*; D007700:Kinetics; D008871:Microvilli / Q000378:metabolism; D011188:Potassium / Q000494:pharmacology*; D011817:Rabbits; D012413:Rubidium / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology*
D005971:Glutamates; D018698:Glutamic Acid; D012964:Sodium; D012413:Rubidium; D011188:Potassium