AJP - Gastrointestinal and Liver Physiology, Vol 261, Issue 3 451-G457, Copyright © 1991 by American Physiological Society
Mechanism of arachidonic acid transport across rabbit distal colonic mucosa
V. Calderaro, B. De Simone, A. Giovane, L. Quagliuolo, L. Servillo, C. Giordano and C. Balestrieri
Institute of Internal Medicine and Nephrology, University of Naples, Italy.
The initial rate of [1-14C]arachidonic acid (AA) entry in the serosal side
of rabbit distal colonic mucosa mounted in Ussing-type chambers is linear
and independent of intracellular metabolism. When the maximal AA uptake was
plotted as a function of medium AA concentration in ranges between 50 and
500 nM, saturation of the AA uptake with increasing concentrations was
observed. The time course of the uptake of oleic acid and palmitic acid was
similar to that observed with AA, and their separate addition to incubation
medium strongly reduced the AA uptake. The influx of arachidonate was
largely inhibited by ouabain and by incubation with mucosal sodium-free
solution and amiloride, while it was increased when colonic mucosa was
exposed to luminal amphotericin B. However, voltage-clamp studies showed
that the AA entry rate appeared to be linearly related (r = 0.99) to
transepithelial potential difference (PD) and suggested that the sodium
dependence of AA translocation is an indirect effect of the changes in
transepithelial PD induced by sodium transport shifts. These features
provide evidence that there is a common entry pathway for AA and other
long-chain free fatty acids mediated by a mechanism of facilitated
diffusion driven by transmembrane PD.
