Cholecystokinin potently releases somatostatin from canine fundic mucosal cells in short-term culture

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Abstract
Gastrin-17 (G-17) and the octapeptide of colecystokinin (CCK-8) were equally potent in their interaction with receptors for 125I-[Leu15]G-17 on isolated canine parietal cells. This was inconsistent with the poor efficacy of CCK-8 compared with G-17 as stimuli of acid secretion in dogs. The effects of G-17and CCK-8 was examined on the release of somatostatinlike immunoreactivity (SLI) from a fraction of small canine fundic mucosal cells separated by elutriation and placed in short-term culture. CCK-8 was considerably more potent and more effective than G-17 in inhibiting 125I-[Leu15]G-17 binding to receptors in the same elutriator fraction. The poor efficacy of CCK compared with G-17 as a stimulant of acid secretion may reflect pronounced activation of somatostatin-mediated acid-inhibitory mechanisms by CCK-8. Differences in affinity between CCK-8 and G-17 at the 125I-[Leu15]G-17 receptor probably do not account for the greater efficacy of CCK-8; the receptor or cell activation mechanisms underlying this greater efficacy of CCK-8 on SLI release remain to be elucidated.