Lenz H J, Klapdor R, Hester S E, Webb V J, Galyean R F, Rivier J E, Brown M R
Gastroenterology. 1986 Oct;91(4):905-12. doi: 10.1016/0016-5085(86)90693-1.
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.
我们研究了向清醒犬脑室内注射30种肽对基础胃酸分泌以及对五肽胃泌素刺激（皮下注射8微克/千克）胃酸分泌的影响。这些肽均未显著增加基础胃酸分泌。12种肽（2纳摩尔/千克）显著（p<0.01）降低了五肽胃泌素刺激的2小时胃酸分泌量（括号内为抑制百分比）：人降钙素（CT）（36%）、神经降压素（NT）（52%）、大鼠促肾上腺皮质激素释放因子（CRF）（59%）、人降钙素基因相关肽（CGRP）（59%）、羊CRF（66%）、β-内啡肽（β-End）（80%）、尾加压素-I（81%）、大鼠CT（81%）、猪胃泌素释放肽（GRP）（83%）、蛙皮素（Svg）（85%）、大鼠CGRP（87%）和蛙皮素（Bom）（95%）。用氯异吲哚铵阻断自主神经系统可消除CRF、β-End、CT和NT诱导的胃抑制作用，但不能消除CGRP和Bom（各1纳摩尔/千克）诱导的胃抑制作用。促肾上腺皮质激素释放因子、β-End、CT、NT、CGRP和Bom显著抑制了由胃内8%蛋白胨餐刺激的2小时胃酸分泌。与对照实验相比，这六种肽均未显著改变蛋白胨餐刺激后血浆胃泌素浓度。在向动物脑室内注射这四种肽后，通过放射免疫测定未检测到胃泌素、CT、CRF和CGRP血浆浓度升高。本研究结果表明，CT、CGRP、NT、β-End以及CRF和Bom家族的肽在脑内发挥作用，抑制清醒犬五肽胃泌素和食物刺激的胃酸分泌。向犬脑室内注射的30种肽均未增加基础胃酸分泌。CRF、β-End、CT和NT诱导的胃酸分泌抑制作用是由自主神经系统介导的，而CGRP和Bom诱导的胃酸分泌抑制作用并非如此。胃泌素似乎在研究的六种脑肽诱导的胃酸抑制中不起作用。
