AJP - Cell Physiology, Vol 255, Issue 4 C486-C494, Copyright © 1988 by American Physiological Society
Na+-coupled sugar transport: membrane potential-dependent Km and Ki for Na+
G. A. Kimmich and J. Randles
Department of Biochemistry, School of Medicine and Dentistry, University of Rochester, New York 14642.
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.
