BILE-SALTS STIMULATE MUCOUS GLYCOPROTEIN-SECRETION FROM CULTURED RABBIT GASTRIC-MUCOSAL CELLS

Resistance of gastric mucosa to damage is increased offer exposure to mild irritants such as bile salts (adaptive cytoprotection). Mucus sec retion also contributes to gastric cytoprotection. We investigated whe ther bile salts stimulate mucous glycoprotein secretion from cultured rabbit gastric mucosal cells. Because prostaglandins (PGs) stimulate m ucus secretion, we assessed she role of endogenous PG release in bile salt-stimulated mucus secretion. Because Ca2+ plays a role in PGE, rel ease, the role of extracellular Ca2+ on PGE, release and mucus secreti on by bile salts was also studied. Rabbit gastric mucosal cells were p repared with collagenase and ethylenediaminetetraacetic acid. These ce lls were cultured as described previously. Cytotoxicity of bile salts was quantified by measuring chromium 51 release from prelabaled cells. PGE, was measured by radioimmunoassay. Mucous glycoprotein secretion was assessed by tritiated glucosamine release assay. Deoxycholate (DC) and glycodeoxycholate (GDC) stimulated tritiated glucosamine release in doses that were not cytotoxic to the cultured cells. DC stimulated PGE, release that was blocked by deprivation of extracellular Ca2+. GD C did not stimulate PGE, release. Neither DC-stimulated nor GDC-stimul ated mucus secretion was affected by indomethacin. Deprivation of extr acellular Ca2+ did not affect DC-stimulated or GDC-stimulated mucus se cretion. Bile salts stimulated mucous glycoprotein secretion from cult ured rabbit gastric mucosal cells. This effect occurred independently of changes in endogenous PGE(2) or extracellular Ca2+ concentrations.