Release of somatostatinlike immunoreactivity from canine fundic mucosal cells in primary culture

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Abstract
A model was developed to allow study of the release of somatostatin-like immunoreactivity (SLI) from gastric mucosal cells. Collagenase-dispersed canine fundic mucosal cells were separated by counterflow elutriation. SLI-containing cells were identified in the fractions with small cells (9-11 .mu.m), and these fractions were plated onto collagen. After 2 days in culture, SLI content of the cells was maintained; SLI-positive cells, detected by peroxidase-antiperoxidase immunohistochemistry, comprised 70 .+-. 6% (mean .+-. SE, n = 6) of these cultured cells. Release of SLI from these cultures into the medium was determined by radioimmunoassay. Epinephrine, dibutyryl cAMP and gastrin each stimulated SLI release in a time-dependent manner, with a steady rate of secretion maintained for 120 min of incubation. Epinephrine and dibutyryl cAMP markedly potentiated the release of SLI stimulated by gastrin but were not themselves mutually potentiating. Upon Sephadex G-50 column chromatography of incubation medium and extracts of cultured cells, SLI eluted primarily in a single peak that cochromatographed with synthetic somatostatin tetradecapeptide. Gastrin and adrenergic stimuli apparently act directly on canine fundic somatostatin cells and potentiating interactions between secretagogues may be important modulating elements in somatostatin cell secretory function.