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Calcitonin gene-related peptide stimulates rat gastric somatostatin release in vitro
Authors:H Koop  R Eissele  V Kühlkamp  E Bothe  J Dionysius  R Arnold
Affiliation:1. Epilepsy Centre, Department of Systems Medicine, University of Rome ‘Tor Vergata”, Rome, Italy;2. Epilepsy Centre, Department of Neuroscience Imaging and Clinical Sciences, “G. D’Annunzio” University of Chieti-Pescara, Italy;3. Epilepsy Centre, Neurologic Unit, SS. Giovanni e Paolo Hospital, Venice, Italy;4. Neurological Clinic and Stroke Unit, “A. Cardarelli” Hospital, Naples, Italy;5. Outpatient Clinic for Epilepsy, “A. Cardarelli” Hospital, Naples, Italy;6. Neurology Unit, University Hospital of Rome “Tor Vergata”, Rome, Italy;7. UOC Neurology, “A. Cardarelli” Hospital, Naples, Italy;8. IRCCS Fondazione Santa Lucia, Rome, Italy;1. Department of Gastroenterology and Hepatology, Mayo Clinic Arizona, Scottsdale, AZ, United States;2. Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA, United States
Abstract:The influence of rat calcitonin gene-related peptide (rCGRP) on the secretion of gastric somatostatin and gastrin was studied in vitro using the isolated, vascularly perfused rat stomach preparation. rCGRP stimulated somatostatin secretion dose-dependently reaching 3-fold stimulation at 1 microM. The kinetics of somatostatin response were characterized by a sharp increase in the initial phase of rCGRP perfusion followed by sustained elevated levels. Gastrin secretion was moderately suppressed at 1 nM to 100 nM CGRP. Somatostatin responses to half-maximal stimulation with 100 nM CGRP were not affected by concomitant perfusion of atropine, propranolol, and tetrodotoxin. It is concluded that increases in somatostatin release in response to CGRP are probably due to a direct effect on the gastric somatostatin-producing D-cell and may be important for the potent acid-inhibitory activity of CGRP.
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