Gastrin stimulation of isolated gastric glands.
Gastrin stimulation of isolated gastric glands.
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胃泌素刺激离体胃腺。
DOI：
10.1152/ajpgi.1982.242.5.g504
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Hersey,SJ
中科院分区：
文献类型：
--
作者：
Chew,CS;Hersey,SJ
在从兔胃粘膜获得的胃腺和分离的壁细胞中研究了胃泌素刺激酸形成的能力。弱碱性氨基比林的积累和耗氧量的增加被用作酸分泌活性的测量。发现对胃泌素的反应非常小（增加10-15%）。然而，包括二硫苏糖醇（0.5 mM）在孵育培养基中增强了腺体和分离的细胞的反应，很容易检测到的水平。对于胃腺制备，胃泌素刺激在1 × 10（-7）M时最大，表观ED 50为5 nM。反应在约30分钟时达到最大值，并稳定至少1小时。胃泌素反应增强磷酸二酯酶抑制剂异丁基甲基黄嘌呤和部分抑制西咪替丁，组胺H2受体拮抗剂。胃泌素和组胺的组合显示出在很宽的组胺浓度范围内的相加反应。然而，时间过程的研究表明，组胺，这达到了高峰，并减少到30分钟的加法响应的胃泌素反应的瞬时增强。使用分离的细胞群丰富的壁细胞（约70%）的研究表明，胃泌素刺激，不抑制西咪替丁。在分离的细胞制剂中也发现组胺对胃泌素反应的瞬时增强作用。胃泌素对细胞cAMP水平或腺苷酸环化酶活性没有影响。结果被解释为表明胃泌素通过三种独立的作用刺激酸分泌：1）直接刺激壁细胞活性，2）与组胺的增强相互作用，和3）对于更完整的制剂，组胺的释放，其反过来作为旁分泌刺激。从数量上看，最重要的作用似乎是组胺的释放。胃泌素的任何作用似乎都不涉及cAMP代谢的变化。
The ability of gastrin to stimulate acid formation was studied in gastric glands and isolated parietal cells obtained from rabbit gastric mucosa. Accumulation of the weak base aminopyrine and increases in oxygen consumption were used as measures of acid secretory activity. The responses to gastrin were found to be very small (10-15% increase). However, inclusion of dithiothreitol (0.5 mM) in the incubation medium enhanced the responses in both glands and isolated cells to easily detectable levels. For the gastric gland preparation, gastrin stimulation was maximal at 1 X 10(-7) M, with an apparent ED50 of 5 nM. The response reached a maximum at about 30 min and was stable for at least an hour. The gastrin response was enhanced by the phosphodiesterase inhibitor isobutylmethylxanthine and partially inhibited by cimetidine, a histamine H2-receptor antagonist. Combinations of gastrin and histamine showed an additive response over a wide range of histamine concentrations. However, time-course studies revealed a transient potentiation of gastrin response by histamine, which reached a peak at 15 min and was reduced to an additive response by 30 min. Studies using isolated cell populations enriched in parietal cells (approximately 70%) revealed a gastrin stimulation that was not inhibited by cimetidine. The transient potentiation of the gastrin response by histamine was also found in the isolated cell preparation. Gastrin had no effect on cellular cAMP levels or adenylyl cyclase activity. The results are interpreted to indicate that gastrin stimulates acid secretion through three separate actions: 1) a direct stimulation of parietal cell activity, 2) a potentiating interaction with histamine, and 3) for more intact preparations, a release of histamine, which in turn acts as a paracrine stimulus. Quantitatively, the most important action appears to be the release of histamine. None of the actions of gastrin appear to involve a change in cAMP metabolism.
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