Prostaglandin stimulates Cl(-)-HCO3- exchange in amphibian oxynticopeptic cells.
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.
Yanaka
A
A
Department of Surgery, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts.
Carter
K J
KJ
Goddard
P J
PJ
Silen
W
W
D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism*; D027963:Chloride-Bicarbonate Antiporters; D004594:Electrophysiology; D005748:Gastric Fundus / Q000378:metabolism; D006706:Homeostasis; D006851:Hydrochloric Acid / Q000494:pharmacology; D006859:Hydrogen / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D007213:Indomethacin / Q000494:pharmacology; D009853:Omeprazole / Q000494:pharmacology; D010295:Parietal Cells, Gastric / Q000378:metabolism* / Q000502:physiology; D011453:Prostaglandins / Q000494:pharmacology*; D011892:Rana catesbeiana; D012146:Rest
D002352:Carrier Proteins; D027963:Chloride-Bicarbonate Antiporters; D011453:Prostaglandins; D006859:Hydrogen; D009853:Omeprazole; D006851:Hydrochloric Acid; D007213:Indomethacin