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JBC, Vol. 270, Issue 19, 11051-11054, May, 1995
VM Rajendran, J Geibel and HJ Binder
The mechanism of sodium movement across apical membrane of colonic crypt
cells of rat distal colon was examined in studies of both 22Na uptake by
apical membrane vesicles (AMV) and the rate of intracellular pH (pHi)
recovery from an acid load by the addition of lumen sodium. In the presence
of chloride but not in its absence, 22Na uptake in crypt AMV was stimulated
by an outward gradient of either [H+] or [Na+]. 22Na uptake stimulated by
an outward [Na+] gradient was also observed in the presence of other
halides in the order of chloride > bromide > fluoride > iodide.
pHi recovery from an acid load was both lumen sodium- and
chloride-dependent, and the rate of pHi recovery by lumen sodium in the
presence of chloride was 65-fold greater than that in the absence of
chloride (dpH/dt is 655.4 and 10.2 in the presence and absence of chloride,
respectively). One mM amiloride inhibited both [H+] gradient- stimulated
22Na uptake in the presence of chloride in crypt AMV (80%) and lumen
sodium- and chloride-dependent pHi recovery in crypt cells (96%). [H+]
gradient stimulation of 22Na uptake by crypt AMV in the presence of
chloride was less sensitive to amiloride than amiloride inhibition of Na-H
exchange in colonic surface AMV. These studies provide compelling evidence
that a chloride-dependent Na-H exchange that is relatively
amiloride-resistant is present in the apical membrane of colonic crypt
cells. As prior studies have not identified a chloride-dependent Na-H
exchange, the molecular and functional basis of this novel transport
process is not known.
Chloride-dependent Na-H exchange. A novel mechanism of sodium transport in colonic crypts
Department of Internal Medicine, Yale University, New Haven, Connecticut 06520, USA.
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