Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/13571
Title: Cholecystokinin (CCK) regulates somatostatin secretion through both the CCK-A and CCK-B/gastrin receptors in sheep.
Authors: Zavros, Y;Shulkes, Arthur
Affiliation: Department of Surgery, University of Melbourne Austin and Repatriation Medical Centre, Victoria, Australia.
Issue Date: 15-Dec-1997
Citation: The Journal of Physiology; 505 ( Pt 3)(): 811-21
Abstract: 1. Cholecystokinin (CCK) and gastrin both stimulate gastric somatostatin (SOM) secretion in vitro and thus have the potential to modulate their direct effects on the parietal cell. However, the relative potencies and the mechanisms of action of CCK and gastrin on SOM secretion in vivo have not been determined. 2. The objectives of the present study were to compare the in vivo potencies of the sulphated(s) and non-sulphated (ns) forms of gastrin heptadecapeptide (G-17) and CCK octapeptide (CCK-8) on SOM secretion, and to determine the nature of the receptors involved by repeating the studies in the presence of the CCK-A and CCK-B/gastrin receptor antagonists L-364,718 and L-365,260, respectively. All experiments were performed in the chronically cannulated sheep. 3. Dose-response experiments revealed the following potencies for SOM secretion: G-17s = CCK-8s > G-17 ns > CCK-8ns. However, based on the plasma levels achieved and a higher metabolic clearance rate (MCR) for CCK, CCK-8s was the most potent. 4. Both the CCK-A and CCK-B/gastrin receptor antagonists suppressed CCK-8s-stimulated SOM output. In contrast, G-17s-stimulated SOM output was inhibited by only the CCK-B/gastrin receptor antagonist. 5. Both receptor antagonists increased basal plasma gastrin and CCK levels. 6. The predominant circulating SOM molecular form after both gastrin and CCK stimulation was SOM-14. 7. In conclusion, the sulphated forms of CCK and gastrin are more potent than the non-sulphated forms. Despite sharing a common biologically active carboxy terminus, CCK stimulates SOM secretion by both the CCK-A and CCK-B/gastrin receptors, while gastrin acts via the CCK-B/gastrin receptor alone. These findings explain in part why CCK is a net inhibitor of gastric acid secretion in vivo.
Internal ID Number: 9457654
URI: http://ahro.austin.org.au/austinjspui/handle/1/13571
URL: http://www.ncbi.nlm.nih.gov/pubmed/9457654
Type: Journal Article
Subjects: Animals
Benzodiazepinones.pharmacology
Cholecystokinin.blood.physiology
Chromatography, High Pressure Liquid
Devazepide
Drug Interactions
Gastric Mucosa.drug effects.secretion
Gastrins.blood.pharmacology
Hormone Antagonists.pharmacology
Infusions, Intravenous
Phenylurea Compounds
Receptor, Cholecystokinin A
Receptor, Cholecystokinin B
Receptors, Cholecystokinin.antagonists & inhibitors.physiology
Sheep
Sincalide.pharmacology
Somatostatin.chemistry.secretion
Appears in Collections:Journal articles

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