Pathophysiology of gastrin and secretin.

The history of gastrin began in 1905 when Edkins observed than an extract of gastric antral mucosa proved to have extraordinary potency in stimulating gastric acid secretion. Approximately 60 years later gastrin was isolated and characterised by Gregory and Tracy (1964). It is composed of a single peptide chain of 17 amino-acids (G17) with a molecular weight of 2100. Two forms of gastrin, I and II, were recognised initially, the only difference being that in II the tyrosyl residue in position 12 is sulphated. The synthesis of human gastrin was achieved by Morley in 1968. The predominant biological activity of gastrin is that of increasing gastric acid production. Several other roles have been assigned to it including trophic effects on the stomach, effects on the exocrine pancreas, and on the enteroinsular axis, but they do not appear to play a role in pathological processes and will not be discussed further. Gastrin is an antral hormone secreted by 'G cells' in the mid zone of the glands. However, smaller amounts of gastrin are present in the duodenum and jejunum and, in some species, there may be small amounts in the pancreas. Recently a substance which reacts with antigastrin antiserum has been detected in the central nervous system (Vanderhaeghen et al., 1975). Immunochemical evidence so far suggests that the 'brain gastrin' consists of COOH terminal fragments of cholecystokinin (Dockray, 1976). The reason for the existence of gastrin-like peptides in the central nervous system is not known and so far they have not been shown to play a role in any pathological process in man.