Cholecystokinin potently releases somatostatin from canine fundic mucosal cells in short-term culture.
Previous studies indicated that 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. These findings were inconsistent with the poor efficacy of CCK-8 compared with G-17 as stimuli of acid secretion in dogs. The present study examines the effects of G-17 and CCK-8 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 as a stimulant of SLI release from these cultured cells. CCK-8 was slightly more potent than G-17 in inhibiting 125I-[Leu15]G-17 binding to receptors in the same elutriator fraction. Our present findings support the hypothesis that 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. The present data indicate that 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.
Soll
A H
AH
Amirian
D A
DA
Park
J
J
Elashoff
J D
JD
Yamada
T
T
D000818:Animals; D002478:Cells, Cultured; D004285:Dogs; D004837:Epinephrine / Q000494:pharmacology; D005748:Gastric Fundus / Q000187:drug effects / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism*; D005755:Gastrins / Q000494:pharmacology; D012844:Sincalide / Q000494:pharmacology*; D013004:Somatostatin / Q000378:metabolism*; D013997:Time Factors
D005755:Gastrins; D013004:Somatostatin; C013550:gastrin 17; D012844:Sincalide; D004837:Epinephrine