胆囊收缩素相关肽对兔胃腺酸生成的抑制及生长抑素释放的刺激作用

Inhibition of acid formation and stimulation of somatostatin release by cholecystokinin-related peptides in rabbit gastric glands.

作者信息

Bengtsson P, Lundqvist G, Nilsson G

机构信息

Department of Physiology, Faculty of Veterinary Medicine, Swedish University of Agricultural Sciences, Uppsala, Sweden.

出版信息

J Physiol. 1989 Dec;419:765-74. doi: 10.1113/jphysiol.1989.sp017897.

DOI:10.1113/jphysiol.1989.sp017897

PMID:2576071

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1190032/

Abstract

The purpose of the present study was to investigate the role of somatostatin in the inhibition of acid production induced by caerulein and cholecystokinin (CCK) in isolated rabbit gastric glands. Acid production was estimated by the aminopyrine technique. 2. Exogenous somatostatin 14 and somatostatin 28 (10(-7) M) reduced to a similar extent the aminopyrine uptake produced by 5 x 10(-5) M-histamine during the course of 40 min incubation. 3. Significant inhibition of histamine-stimulated aminopyrine accumulation occurred at a somatostatin 14 concentration of 10(-9) M. 4. Caerulein and CCK octapeptide (10(-13)-10(-7) M) were found to release somatostatin from isolated gastric glands in a dose-dependent manner. The dose-response relationships for somatostatin release and inhibition of aminopyrine uptake were similar. Thus, the half-maximal dose approximations for somatostatin release and inhibition of aminopyrine uptake were 0.5 and 1.4 x 10(-9) M respectively for CCK octapeptide and 0.9 and 2.5 x 10(-11) M for caerulein. Heptadecapeptide gastrin proved to be a very poor releaser of somatostatin in the system used. The CCK octapeptide-induced somatostatin release was time dependent and the concentrations of somatostatin that accumulated in the incubation medium were similar to those of exogenous somatostatin that were needed to evoke inhibition. 5. The present results support the concept that cholecystokinin inhibits gastric acid secretion by releasing somatostatin from endocrine-like cells in the gastric mucosa. It is suggested that cholecystokinin-related peptides may play a physiological role in inhibiting gastric acid secretion. A similar role for gastrin is not supported by the present study.

摘要

本研究的目的是探讨生长抑素在抑制蛙皮素和胆囊收缩素（CCK）诱导的离体兔胃腺酸分泌中的作用。酸分泌通过氨基比林技术进行评估。2. 在40分钟的孵育过程中，外源性生长抑素14和生长抑素28（10⁻⁷ M）使5×10⁻⁵ M组胺诱导的氨基比林摄取降低到相似程度。3. 当生长抑素14浓度为10⁻⁹ M时，对组胺刺激的氨基比林积累有显著抑制作用。4. 发现蛙皮素和CCK八肽（10⁻¹³ - 10⁻⁷ M）以剂量依赖性方式从离体胃腺释放生长抑素。生长抑素释放和氨基比林摄取抑制的剂量 - 反应关系相似。因此，对于CCK八肽，生长抑素释放和氨基比林摄取抑制的半数最大剂量近似值分别为0.5和1.4×10⁻⁹ M，对于蛙皮素则分别为0.9和2.5×10⁻¹¹ M。在所用系统中，十七肽胃泌素被证明是生长抑素的非常弱的释放剂。CCK八肽诱导的生长抑素释放是时间依赖性的，孵育培养基中积累的生长抑素浓度与引起抑制所需的外源性生长抑素浓度相似。5. 目前的结果支持这样的概念，即胆囊收缩素通过从胃黏膜中的类内分泌细胞释放生长抑素来抑制胃酸分泌。提示胆囊收缩素相关肽可能在抑制胃酸分泌中发挥生理作用。本研究不支持胃泌素具有类似作用。