Neurogastroenterology Laboratory, Departments of Medicine, University of Hamburg, Hamburg, FRG and University of California San Diego, San Diego, California, USA.
J Neuroendocrinol. 1989 Jun 1;1(3):163-7. doi: 10.1111/j.1365-2826.1989.tb00097.x.
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.
摘要 几种肽类物质被认为是调节各种外周器官系统的中枢神经系统递质。本研究检测了大鼠促肾上腺皮质素释放因子（CRF）、鲑鱼降钙素（CT）、β-内啡肽（β-End）、神经降压素（NT）、大鼠降钙素基因相关肽（CGRP）和铃蟾肽（BOM）对清醒犬胃酸分泌、胃排空和胃左动脉血流的中枢神经系统作用。这些肽类物质全部经第三脑室内注射，均显著抑制胃酸分泌，但对蛋白餐刺激的血浆胃泌素浓度无影响。用氯氨酮进行神经节阻滞可消除 CRF、CT、β-End 和 NT 的胃抑制作用，但对 CGRP 和 BOM 无影响。胃左动脉血流的抑制作用仅被迷走神经干切断术阻断，而双侧肾上腺切除术并不影响 6 种肽类物质引起的胃酸抑制。CRF、NT 和 BOM 经脑室内给药可显著延迟蛋白餐的胃排空，而β-End、CT 和 CGRP 则无此作用。只有 BOM 显著增加胃左动脉血流。这些结果表明，各种神经肽以不同的方式和通过不同的途径改变胃功能。CRF 和 CT 通过激活交感传出纤维抑制进食刺激的胃酸分泌。β-End 和 NT 通过抑制迷走传出纤维抑制进食刺激的胃酸分泌，而介导 CT 和 CGRP 引起的犬胃酸抑制的途径尚不清楚。胃泌素、肾上腺和胃排空或血流变化在介导 CRF、CT、β-End、NT、CGRP 和 BOM 脑室内给药引起的胃酸抑制中不起作用。
