Neuroendocrine regulation of canine gastric secretion, emptying and blood flow.

Abstract Several peptides have been implicated as central nervous system transmitters regulating various peripheral organ systems. This study examined the central nervous system effects of rat corticotrophin-releasing factor (CRF), salmon calcitonin (CT), beta-endorphin (beta-End), neurotensin (NT), rat calcitonin gene-related peptide (CGRP) and bombesin (BOM) on gastric acid secretion, gastric emptying and left gastric artery flow in conscious dogs. All of these peptides, injected into the third cerebral ventricle, significantly inhibited gastric acid secretion but not plasma gastrin concentrations stimulated by a liquid protein meal. Ganglionic blockade with chlorisondamine abolished the gastric inhibitory action of CRF, CT, beta-End and NT but not of CGRP and BOM. Truncal, subdiaphragmatic vagotomy prevented the gastric inhibitory actions of beta-End and NT only, while bilateral adrenalectomy did not affect gastric acid inhibition induced by any of the six peptides. Cerebroventricular administration of CRF, NT and BOM significantly delayed gastric emptying of the protein meal while beta-End, CT and CGRP were not effective. Only BOM significantly increased left gastric artery flow. These results indicate that various neuropeptides alter gastric functions in a differentiated fashion and via distinct pathways. CRF and CT inhibit meal-stimulated gastric acid secretion by activation of sympathetic efferents. beta-End and NT inhibit meal-stimulated acid secretion by inhibition of vagal efferents while the pathways that mediate CT- and CGRP-induced gastric acid inhibition in the dog are unknown. Gastrin, the adrenal glands and changes in gastric emptying or blood flow do not play a role in mediating gastric acid inhibition produced by Cerebroventricular administration of CRF, CT, beta-End, NT, CGRP and BOM.