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Intracerebroventricular administration of human calcitonin and human calcitonin gene-related peptide inhibits meal-stimulated gastric acid secretion in the dog
Authors:Dr. H. Jürgen Lenz MD  Dr. Marvin R. Brown MD
Affiliation:(1) Clayton Foundation Laboratories for Peptide Biology, The Salk Institute, 10010 N. Torrey Pines Road, 92037 La Jolla, California;(2) Present address: Department of Medicine, University Hospital Eppendorf, University of Hamburg, Hamburg, Germany;(3) Department of Medicine T-017, UCSD Medical Center, 225 Dickinson Street, 92103-9981 San Diego, California
Abstract:This study was designed to assess the central nervous system actions of human calcitonin (hCalc) and human calcitonin gene-related peptide (hCGRP) on meal-stimulated gastric acid secretion in awake beagle dogs. hCalc (0.1–1.0 nmol/kg) and hCGRP (0.01–1.0 nmol/kg) injected into the third cerebral ventricle significantly inhibited gastric acid secretion stimulated by an 8% peptone meal. hCGRP was ten times more potent than hCalc in inhibiting gastric secretion. Neither hCalc nor hCGRP significantly altered plasma gastrin concentrations compared to control values. Truncal vagotomy did not prevent the gastric inhibitory actions of hCalc and hCGRP. Ganglionic blockade with chlorisondamine completely abolished the gastric inhibitory action of hCalc but had no effect on gastric acid inhibition induced by hCGRP. The results of this study indicate that intracerebroventricular administration of hCalc and hCGRP inhibits meal-stimulated gastric acid secretion in awake dogs. Inhibition of gastric acid secretion by hCalc and hCGRP in the dog is not mediated by inhibition of gastrin release or by the vagus nerves. Human Calc but not human CGRP appears to inhibit meal-stimulated gastric acid secretion in the dog by activation of the autonomic (sympathetic) nervous system.
Keywords:calcitonin  calcitonin gene-related peptide  gastric secretion
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