DISTINCT EFFECTS OF TETRAGASTRIN, HISTAMINE, AND CCH ON RAT GASTRIC MUCIN SYNTHESIS AND CONTRIBUTION OF NO

Although gastrin, histamine, and carbachol (CCh) accelerate gastric mu cin metabolism, information about their target cells of mucin producti on is lacking. To clarify this, we examined the effects of these stimu lants, including the possible participation of nitric oxide (NO), on m ucin biosynthesis in distinct sites and layers of rat gastric mucosa. Pieces of tissue obtained from the corpus and antrum were incubated in a medium containing radioactive precursors and each stimulant, with o r without NO synthase (NOS) inhibitor. Distribution of NOS was compare d with that of the specific mucins by immunostaining using specific an tiserum and monoclonal antibodies. In the full-thickness corpus mucosa , tetragastrin enhanced [H-3]glucosamine incorporation into mucin but had no effect on [C-14]threonine incorporation. Both histamine and CCh dose dependently increased H-3- and C-14-labeled corpus mucin. Only C Ch stimulated antral mucin biosynthesis. CCh stimulation was noted in the corpus mucosa after removal of surface mucous cells, but stimulati on by tetragastrin or histamine disappeared as a result of this pretre atment. Only tetragastrin-induced activation was completely blocked by the NOS inhibitor. NOS immunoreactivity was limited to surface mucous cells. Mucus-producing cells present in the different sites and layer s of the gastric mucosa have distinct mechanisms for regulation of muc in biosynthesis. Gastrin-stimulated mucin biosynthesis mediated by NO is limited to surface mucous cells of rat gastric oxyntic mucosa.