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Prostaglandins alter the relationship between gastric hydrogen ion concentration and flow: evidence for stimulation of non‐parietal secretion in the cat
Author(s) -
Gascoigne A. D.,
Hirst B. H.
Publication year - 1981
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1981.sp013798
Subject(s) - stimulation , secretion , parietal cell , hydrogen ion , gastric secretion , endocrinology , medicine , chemistry , gastric acid , biology , ion , organic chemistry
1. The effect of i.v. administration of prostaglandin (PG) E 2 (10‐40 μg kg −1 h −1 ), 16,16‐dimethyl PGE 2 (0·1‐0·5 μg kg −1 h −1 ), PGE 1 (16‐20 μg kg −1 h −1 ), PGA 1 (5‐11 μg kg −1 h −1 ) and PGF 2α (40 μg kg −1 h −1 ) on the relationship between [H + ] and flow of gastric juice during stimulation of gastric secretion by pentagastrin was investigated in conscious cats prepared with cannulated gastric fistulae. 2. A‐ and E‐type prostaglandins significantly reduced pentagastrin‐stimulated acid output. This inhibition was associated with a reduction of the [H + ] of the gastric juice such that the [H + ] observed at any flow rate tended to be lower than the normal range observed with pentagastrin alone. With the highest doses of these prostaglandins the mean [H + ] values were well below the normal range with pentagastrin alone. 3. At the dose tested, PGF 2α had little effect on acid output, and did not alter the relationship between [H + ] and gastric flow. 4. There is a linear relationship between acid output and gastric flow and this relationship is similar during stimulation of gastric secretion by pentagastrin, histamine or insulin. Gastric acid inhibitory doses of cimetidine, atropine and somatostatin did not alter this relationship. In contrast the A‐ and E‐type prostaglandins displaced this relationship to the right of the normal line observed with the acid stimulants alone. A‐ and E‐type prostaglandins reduced the slope of the line relating acid output and gastric flow from ∼ 150‐170 μequiv/ml −1 to ∼ 100‐120 μequiv ml −1 , this being taken as evidence of dilution of the parietal H + secretion with a non‐parietal secretion. 5. The volume of non‐parietal gastric secretion was calculated as the gastric flow at zero acid output by extrapolation of linear plots of acid output versus gastric flow. Unstimulated gastric flow measured directly was 0·75 ml 15 min −1 . The calculated non‐parietal flow was in the range 0·52‐0·90 ml 15 min −1 during stimulation of gastric secretion with pentagastrin, histamine and insulin, and inhibition of pentagastrin‐stimulated acid secretion with cimetidine, atropine and somatostatin. PGE 2 (1·51 ml 15 min −1 ) and 16,16‐dimethyl PGE 2 (1·20 ml 15 min −1 ) nearly doubled the calculated non‐parietal flow. 6. These data demonstrate that gastric acid inhibitory doses of A‐ and E‐type prostaglandins can reduce the [H + ] in the bulk fluid of the gastric lumen during stimulation of acid secretion. The data provide evidence that these prostaglandins stimulate a non‐parietal component of gastric secretion. This might be gastric bicarbonate and mucus secretion.