Pepsin 1 secretion in chronic peptic ulceration. Gut

SUMMARY In patients with peptic ulceration, both vagal stimulation by insulin hypoglycaemia and stimulation by pentagastrin cause pepsin 1 to be secreted into gastric juice. There is a secretory threshold for pepsin 1, below which only pepsins 3 and 5 are secreted. Pepsin 1 accounts for an increasing proportion of the total peptic activity/ml of gastric juice as the total activity increases. Higher concentrations of pepsin 1 in the basal gastric secretion occurred significantly more frequently in patients with duodenal ulcer than with gastric ulcer. In these patients there may be an increased 'background ' secretory drive. On agar gel electrophoresis of normal human gastric juice at ph 5.0, up to eight zones of proteolytic activity may be recognised, at least five of which represent unique pepsins. ' Using the nomenclature suggested by these authors,2 the pepsins are num-bered 1, 2, 3a, 3, and 5 in order of electrophoretic mobility to the anode with reference to a porcine pepsin marker. Pepsin 3 is always the most abundant of the pepsins present, usually followed by pepsin 5. The proportional contribution made by pepsin 1 to the total peptic activity is variable. Taylor3 found that in response to histamine, patients with chronic peptic ulceration secreted pepsin 1 significantly more often and in greater quantity than did control subjects. Vagally stimu-lated gastric secretions were not studied. In the cat, prolonged electrical stimulation of the vagi results in the secretion of increasing amounts of the most electronegative pepsin, 'cat pepsin 1'.4 This observa-tion prompted further study of pepsin 1 secretion by patients with chronic peptic ulceration, both in response to vagal stimulation by insulin hypogly-caemia and to pentagastrin