Na+-coupled sugar transport: membrane potential-dependent Km and Ki for Na+.
Kinetic analysis of the characteristics of phlorizin binding and of the Na+, sugar, and potential dependence of alpha-methylglucoside (alpha-MG) influx into isolated avian intestinal cells has pointed toward two alternative models for the transport mechanism (D. Restrepo and G. A. Kimmich, J. Membr. Biol. 89: 269-280, 1986). One of these models envisions a potential-dependent Na+ binding event (Na+ well concept) as a part of the molecular mechanism. The data reported here show that the apparent Km for Na+ for sugar transport is sharply dependent on the magnitude of the membrane potential. When intracellular Na+ is absent, the maximal velocity (Vmax) achieved for sugar influx is the same with or without a potential, although Vmax is obtained at a lower Na+ concentration when a potential is imposed (interior negative). Intracellular Na+ severely inhibits the influx of sugar in the absence of a potential, but this effect is largely overcome when a potential is present. The Vmax obtained when intracellular Na+ is present is a function of the potential. These results are consistent with a transport model in which Na+ binding to the Na+-dependent sugar carrier at the extracellular surface of the membrane and debinding at the inner surface of the membrane are both potential-dependent events.
Kimmich
G A
GA
Department of Biochemistry, School of Medicine and Dentistry, University of Rochester, New York 14642.
Randles
J
J
D000818:Animals; D001693:Biological Transport, Active; D002645:Chickens; D004848:Epithelium / Q000502:physiology; D007422:Intestines / Q000502:physiology*; D007700:Kinetics; D008564:Membrane Potentials; D008757:Methylglucosides / Q000378:metabolism*; D008759:Methylglycosides / Q000378:metabolism*; D008954:Models, Biological; D012964:Sodium / Q000378:metabolism* / Q000494:pharmacology
D008757:Methylglucosides; D008759:Methylglycosides; C027020:methylglucoside; D012964:Sodium