Inhibition of gastric acid secretion by brain peptides in the dog. Role of the autonomic nervous system and gastrin.
We have studied the effects of 30 peptides administered intracerebroventricularly on basal and pentagastrin-stimulated (8 micrograms/kg s.c.) gastric acid secretion in conscious dogs. None of the peptides significantly increased basal gastric acid secretion. Twelve peptides (2 nmol/kg) significantly (p less than 0.01) decreased the pentagastrin-stimulated 2-h acid output (percentage inhibition in parentheses): human calcitonin (CT) (36%), neurotensin (NT) (52%), rat corticotropin-releasing factor (CRF) (59%), human calcitonin gene-related peptide (CGRP) (59%), ovine CRF (66%), beta-endorphin (beta-End) (80%), urotensin-I (81%), rat CT (81%), porcine gastrin-releasing peptide (GRP) (83%), sauvagine (Svg) (85%), rat CGRP (87%), and bombesin (Bom) (95%). Blockade of the autonomic nervous system with chlorisondamine abolished the gastric inhibitory action induced by CRF, beta-End, CT, and NT, but not by CGRP and Bom (1 nmol/kg each). Corticotropin-releasing factor, beta-End, CT, NT, CGRP, and Bom significantly inhibited gastric acid secretion stimulated by an intragastric 8% peptone meal for 2 h. None of these six peptides significantly altered plasma gastrin concentrations in response to the peptone meal as compared with control experiments. A rise of plasma concentrations of gastrin, CT, CRF, and CGRP could not be detected by radioimmunoassay in animals after intracerebroventricular administration of these four peptides. The results of this study indicate that CT, CGRP, NT, beta-End, and peptides of the CRF and Bom families act within the brain to inhibit pentagastrin- and meal-stimulated gastric acid secretion in conscious dogs. None of the 30 peptides administered intracerebroventricularly increased basal gastric acid secretion in the dog. Inhibition of gastric acid secretion induced by CRF, beta-End, CT, and NT, but not by CGRP and Bom is mediated by the autonomic nervous system. Gastrin does not appear to play a role in gastric acid inhibition induced by the six brain peptides studied.
D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology*; D001839:Bombesin / Q000494:pharmacology; D001921:Brain / Q000378:metabolism; D002116:Calcitonin / Q000494:pharmacology; D015740:Calcitonin Gene-Related Peptide; D003346:Corticotropin-Releasing Hormone / Q000494:pharmacology; D004285:Dogs; D004723:Endorphins / Q000494:pharmacology; D005744:Gastric Acid / Q000378:metabolism*; D005755:Gastrins / Q000502:physiology*; D007276:Injections, Intraventricular; D008297:Male; D009419:Nerve Tissue Proteins / Q000494:pharmacology; D009496:Neurotensin / Q000494:pharmacology; D010455:Peptides / Q000494:pharmacology*; D001615:beta-Endorphin
D004723:Endorphins; D005755:Gastrins; D009419:Nerve Tissue Proteins; D010455:Peptides; D009496:Neurotensin; D001615:beta-Endorphin; D002116:Calcitonin; D003346:Corticotropin-Releasing Hormone; D015740:Calcitonin Gene-Related Peptide; D001839:Bombesin