title: Effect of somatostatin on cholecystokinin-induced amylase release in rat pancreatic acini.
abstract: The effect of somatostatin on cholecystokinin-induced amylase release was investigated in isolated rat pancreatic acini. Acini were isolated by enzymatic digestion and incubated in a HEPES buffered Ringer's solution with testing reagents for 30 minutes at 37 degrees C. The activity of released amylase, cAMP, and inositol phosphate formation were measured. Intracellular calcium concentration ([Ca2+]i) was also checked. Somatostatin 14 and octreotide, a somatostatin analog, inhibited CCK-stimulated amylase release in a concentration-dependent manner. The inhibitory effect of octreotide on CCK-induced amylase release was not shown when the acini were treated with 8-Br-cAMP, irrespective of the presence of IBMX. Forskolin potentiated CCK-induced amylase release and this effect was blocked by octreotide treatment; although CCK-8 (3 x 10(-11) M) failed to stimulate cAMP formation, octreotide significantly inhibited basal cAMP formation in the acini. The increase of [Ca2+]i in response to CCK was inhibited by octreotide. However, CCK-induced inositol phosphate formation was not changed by 10(-9) M octreotide. Octreotide had no effect on CCK-stimulated tyrosine phosphorylation, and tyrosine phosphatase inhibitors (NaF and Na2WO4) did not influence the effect of octreotide on CCK-induced amylase release. From these results, we conclude that octreotide inhibits CCK-induced amylase release by inhibiting basal cAMP formation and decreasing the [Ca2+]i stimulated by CCK.
authors.affiliation: Department of Physiology, College of Medicine, The Catholic University of Korea, Socho-gu, Seoul.
authors.forename: D J
authors.initials: DJ
authors.lastname: Rhie
authors.forename: M J
authors.initials: MJ
authors.lastname: Kim
authors.forename: W S
authors.initials: WS
authors.lastname: Choi
authors.forename: K H
authors.initials: KH
authors.lastname: Lee
authors.forename: J H
authors.initials: JH
authors.lastname: Sung
authors.forename: D S
authors.initials: DS
authors.lastname: Min
authors.forename: S H
authors.initials: SH
authors.lastname: Yoon
authors.forename: S J
authors.initials: SJ
authors.lastname: Hahn
authors.forename: M S
authors.initials: MS
authors.lastname: Kim
authors.forename: Y H
authors.initials: YH
authors.lastname: Jo
mesh_terms: D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000681:Amylases / Q000378:metabolism*; D000818:Animals; D020013:Calcium Signaling / Q000187:drug effects; D002474:Cell-Free System; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000096:biosynthesis; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007295:Inositol Phosphates / Q000096:biosynthesis; D020935:MAP Kinase Signaling System / Q000187:drug effects; D015282:Octreotide / Q000494:pharmacology; D010179:Pancreas / Q000187:drug effects* / Q000378:metabolism; D017027:Protein Tyrosine Phosphatases / Q000037:antagonists & inhibitors / Q000502:physiology; D051381:Rats; D015290:Second Messenger Systems / Q000187:drug effects*; D012636:Secretory Rate / Q000187:drug effects; D012844:Sincalide / Q000494:pharmacology*; D012969:Sodium Fluoride / Q000494:pharmacology; D013004:Somatostatin / Q000494:pharmacology*; D017973:Tungsten Compounds / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D007295:Inositol Phosphates; D017973:Tungsten Compounds; D005576:Colforsin; D015124:8-Bromo Cyclic Adenosine Monophosphate; D013004:Somatostatin; C025399:sodium tungstate(VI); D012969:Sodium Fluoride; D000242:Cyclic AMP; D017027:Protein Tyrosine Phosphatases; D000681:Amylases; D012844:Sincalide; D015282:Octreotide; D015056:1-Methyl-3-isobutylxanthine