Abstract
Extracts of antral, duodenal and jejunal mucosa contained the same concentrations and molecular forms of gastrin in cat and dog. In both species component III constituted 93%, component II 4% and components I and IV each 1% of the total immunoreactivity. During electrical vagal stimulation or feeding in anesthetized cats with ligated kidney vessels and resected jejunum and ileum, anesthetized normal cats or conscious normal cats, release of the large molecular forms of gastrin, components I and II, was not detectable. Luminal perfusates of cat antrum contained only component III and occasionally less than 2% of component IV. Injections (i.v.) into conscious cats of components I, II and III isolated from cat antrum revealed a significantly slower elimination of the large components (t1/2 [half-life] .apprx. 4.2 and 4.0 min, respectively) than of component III (t1/2 .apprx. 1.1 min). The absence of components I and II in cat blood cannot be due to rapid degradation. During feeding, components I and II constituted 20% of the total gastrin immunoreactivity in antral venous blood of dogs. This amount is sufficient to account for the predominance of large components in peripheral venous blood in dogs considering their slow metabolic clearacne rates. Luminal perfusates of dog antrum contained components I, II and III in proportions corresponding to those found in the antrum. Components I and II are synthesized in the same proportions in cat and dog gastrin cells. In the cat, components I and II are never released from the cells. Since these components contain heptadecapeptide gastrin within their sequences, they probably represent biosynthetic precursors of the principal gastrin, the heptadecapeptide (component III). The predominance of component III in gastric juice suggests that the feline gastrin cell secretes only component III, which degrades to component IV in blood.