Non-parietal Cells Research Articles

Actions of histamine, secretin, and PGE2 on cyclic AMP production by isolated canine fundic mucosal cells.

Cyclic AMP production was studied in isolated canine fundic gastric mucosal cells. Histamine, prostaglandin E2 (PGE2), and secretin increased cyclic AMP production by unenriched mucosal cells. In separated cell fractions, histamine stimulation of cyclic AMP production correlated with the parietal cell content of the fractions. Secretin in concentrations above 1 nM stimulated cyclic AMP production, and this effect correlated with the pepsinogen content of the separated cell fractions. At concentrations above 1 microM, PGE2 stimulated cyclic AMP production; this effect was found in all separated cell fractions and was not associated with any of the available cell markers. PGE2 stimulation of cyclic AMP production was, however, negatively correlated with the parietal cell content. Thus, histamine stimulated cyclic AMP production by parietal cells and secretin stimulated production of cyclic AMP by chief cells. PGE2 stimulation of cyclic AMP production could not be localized to a single cell type but occurred primarily in nonparietal cells.

Stimulation of mucus and nonparietal cell secretion by the E2 prostaglandins.

The effects of prostaglandin E2 (PGE2), 15-methyl prostaglandin E2 (15M), and 16,16-dimethyl prostaglandin E2 (16DM) on gastric mucus and nonparietal cell secretion in rats were measured. Alcian blue binding was used as a measure of gastric mucus. Applied topically, all three agents stimulated nonparietal cell secretion, and PGE2 and 16DM stimulated the secretion of mucus, increasing the fraction in the gastric contents but not that adherent to the mucosa. Topical 15M did not stimulate the production of mucus. Given intranveously, all three agents increased the amount of mucus in the gastric contents without altering the amount of mucus bound to the mucosa. The prostaglandins had no effect on nonparietal cell secretion when given intravenously. These effects could be relevant to the ability of the E2 prostaglandins to protect the gastric mucosa from damage.

Stimulation of non-parietal cell secretion in canine Heidenhain pouches by 16,16-dimethyl prostaglandin E2.

The permeability effects of topical and intravenous prostaglandin E2 (PGE2) and 16,16-dimethyl prostaglandin E2 (16DM) were studied in canine Heidenhain pouches using an acid-free perfusate, and changes in volume and HCO-3 content of the perfusate were measured. Topical and intravenous 16DM increased the apparent flux of Na+ and Cl-, and stimulated the secretion of fluid containing HCO-3. 16DM stimulates non-parietal cell secretion and therefore the movement of Na+ cannot be interpreted as passive flux in response to changes in permeability.

The relationship between acid, pepsin, and electrolytes in gastric juice before and after subcutaneous injection of histamine in man.

The gastric secretion of acid (TA), pepsin (CPU), sodium (Na), potassium (K), and magnesium (Mg), was studied in 14 patients before and after subcutaneous injection of 0.04 mg histamine diphosphate. The concentrations ([]) and outputs (Q) of TA, CPU, and K increased significantly after stimulation with histamine, while the [Mg] and [Na] decreased. The QNa was unchanged by histamine-stimulation, whereas QMg showed a significant increase in the first 20-minute period after histamine-stimulation. A correlation analysis between the parameters showed positive correlations between TA and CPU, TA and K, and a negative correlation between [TA] and [NA] or [Mg], There was a significant positive correlation between Na and Mg, but no significant correlation between CPU and Mg or Na. It is suggested that Mg stems from a different non-parietal cell secretion than pepsin, but that it probably has the same origin as Na.

Histamine Secretory Tests in Cats: An Evaluation of Results Based Upon Hollander's Two-Component Theory

Summary A method is described of performing acute total gastric pouch secretory studies in anesthetized cats. The maximal secretory capacity of the gastric epithelium in these preparations was influenced by the duration of histamine administration as well as the dose. It is possible to obtain a larger output of gastric juice for a short period by doubling the dose of histamine each 2 hours than by giving a larger dose over a prolonged test. The correlations between the ionic concentrations in the stimulated and in the unstimulated cats are on the whole consistent with Hollander's two-component theory of gastric secretion. The composition of the two components differs in the two states, the chief difference being an increase in the K concentration in the nonparietal cell secretion on stimulation, with a corresponding decrease in the K in the parietal cell secretion. Histamine increases the rates of both secretions with a greater increase in the parietal cell secretion. The reason for the K content of parietal secretion, which is at variance with the Hollander theory, is not clear but may be due to species difference, to retained innervation of the stomach or to the anesthetic.