AJP - Gastrointestinal and Liver Physiology, Vol 262, Issue 1 44-G49, Copyright © 1992 by American Physiological Society
Prostaglandin stimulates Cl(-)-HCO3- exchange in amphibian oxynticopeptic cells
A. Yanaka, K. J. Carter, P. J. Goddard and W. Silen
Department of Surgery, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts.
Prostaglandins, shown to stimulate Cl- transport in epithelial cells of
several different tissues, protect gastric mucosa against physiological
injury induced by luminal acid. To clarify the relationship between the
stimulation of Cl(-)-transport and the protection of gastric mucosa, the
effect of prostaglandin on Cl(-)-HCO3- exchange in oxynticopeptic cells
(OPC) was examined in intact sheets of in vitro frog gastric mucosa, in
which OPC were selectively loaded with the pH-sensitive fluorescent dye
2',7'-bis(carboxyethyl)-5(6')-carboxyfluorescein (BCECF). In omeprazole
(0.3 mM)-pretreated frog fundic mucosae, in which H+ secretion was totally
inhibited, 16,16-dimethyl prostaglandin E2 (dmPGE2) induced a significant
decrease in intracellular pH (pHi) in OPC simultaneously with a significant
increase in pHi in adjacent muscularis mucosae, an effect abolished by
removal of ambient Cl- or addition of
4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) (0.5 mM). dmPGE2
accentuated the rates of alkalinization of OPC after either removal of
ambient Cl- or addition of serosal H2DIDS. During exposure to luminal or
serosal acid, dmPGE2 significantly attenuated acidification of OPC induced
by the exogenous H+, effects abolished either by removal of ambient Cl- or
by addition of H2DIDS (0.5 mM). These results suggest that 1) dmPGE2
stimulates extrusion of HCO3- through the basolateral Cl(-)-HCO3- exchanger
in resting OPC (H+ secretion inhibited) and that 2) relatively high
extracellular [HCO3-] on the basolateral surface afforded by dmPGE2
protects OPC from acidification during exposure to luminal or serosal acid.
