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Korean J Gastroenterol. 1998 Dec;32(6):773-781. Korean. Original Article.
Rhie DJ , Choi WS , Yi SY , Yoon SH , Hahn SJ , Sim SS , Kim MS , Jo YH .
Department of Physiology, College of Medicine, The Catholic University of Korea, Seoul, Korea.

BACKGROUND/AIMS: The inhibitory effect of somatostatin (SS) on cholecystokinin (CCK)-induced amylase release and the role of intracellular cAMP in this process were investigated. METHODS: Pancreatic acini were isolated from rat pancreas and treated with solution involving collagenase and then, dispersed. Amylase release was measured. In another set of experiment, cAMP and inosito phosphate (IP) formation were measured. RESULTS: SS-14 inhibited CCK-8-induced amylase release Octreotide, somatostatin analog, also inhibited CCK-8-induced amylase release equipotently. The inhibitory effect of octreotide on CCK-8-induced amylase release was not found in the presence o 8-bromo-cAMP. Forskolin, an adenylyl cyclase activator, potentiated K-8-induced amylase release. However, the amylase release achieved by the simultaneous administration of CCK-8 and octreotide was not altered by forskolin, while the cAMP level in response to the administration of CCK-8 and octreotide was increased significantly by forskolin. Octreotide inhibited the basal cellular cAMP leve significantly, but CCK-8 alone did not exhibit any change. CCK-8-induced IP formation was no changed by octreotide. Tyrosine phosphatase inhibitors did not affect inhibitory action of octreotide on CCK-8-induced amylase release. CONCLUSIONS: From the above results, it is concluded that SS inhibits amylase release induced by CCK in dispersed pancreatic acini of rat. A decrease in pancreatic amylase release in response to octreotide may be attributed to inhibited basal cAMP formation Further study is needed to elucidate the related process.

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