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使用分离的大鼠胃肠嗜铬样细胞对CCK2受体拮抗剂进行药理学分析。

Pharmacological analysis of CCK2 receptor antagonists using isolated rat stomach ECL cells.

作者信息

Lindström E, Björkqvist M, Håkanson R

机构信息

Department of Pharmacology, University of Lund, Sweden.

出版信息

Br J Pharmacol. 1999 May;127(2):530-6. doi: 10.1038/sj.bjp.0702538.

Abstract
  1. Gastrin stimulates rat stomach ECL cells to secrete histamine and pacreastatin, a chromogranin A (CGA)-derived peptide. The present report describes the effect of nine cholecystokinin2 (CCK2) receptor antagonists and one CCK1 receptor antagonist on the gastrin-evoked secretion of pancreastatin from isolated ECL cells. 2. The CCK2 receptor antagonists comprised three benzodiazepine derivatives L-740,093, YM022 and YF476, one ureidoacetamide compound RP73870, one benzimidazole compound JB 93182, one ureidoindoline compound AG041R and three tryptophan dipeptoids PD 134308 (CI988), PD135158 and PD 136450. The CCK1 receptor antagonist was devazepide. 3. A preparation of well-functioning ECL cells (approximately 80% purity) was prepared from rat oxyntic mucosa using counter-flow elutriation. The cells were cultured for 48 h in the presence of 0.1 nM gastrin; they were then washed and incubated with antagonist alone or with various concentrations of antagonist plus 10 nM gastrin (a maximally effective concentration) for 30 min. Gastrin dose-response curves were constructed in the absence or presence of increasing concentrations of antagonist. The amount of pancreastatin secreted was determined by radioimmunoassay. 4. The gastrin-evoked secretion of pancreastatin was inhibited in a dose-dependent manner. YM022, AG041R and YF476 had IC50 values of 0.5, 2.2 and 2.7 nM respectively. L-740,093, JB93182 and RP73870 had IC50 values of 7.8, 9.3 and 9.8 nM, while PD135158, PD136450 and PD134308 had IC50 values of 76, 135 and 145 nM. The CCK1 receptor antagonist devazepide was a poor CCK2 receptor antagonist with an IC50 of about 800 nM. 5. YM022, YF476 and AG041R were chosen for further analysis. YM022 and YF476 shifted the gastrin dose-response curve to the right in a manner suggesting competitive antagonism, while the effects of AG041R could not be explained by simple competitive antagonism. pK(B) values were 11.3 for YM022, 10.8 for YF476 and the apparent pK(B) for AG041R was 10.4.
摘要
  1. 胃泌素刺激大鼠胃肠嗜铬样(ECL)细胞分泌组胺和胰抑制素,后者是一种源自嗜铬粒蛋白A(CGA)的肽。本报告描述了9种胆囊收缩素2(CCK2)受体拮抗剂和1种CCK1受体拮抗剂对胃泌素诱发的离体ECL细胞分泌胰抑制素的影响。2. CCK2受体拮抗剂包括3种苯二氮䓬衍生物L-740,093、YM022和YF476,1种脲基乙酰胺化合物RP73870,1种苯并咪唑化合物JB 93182,1种脲基吲哚啉化合物AG041R以及3种色氨酸二肽类化合物PD 134308(CI988)、PD135158和PD 136450。CCK1受体拮抗剂是地伐西匹。3. 使用逆流淘析法从大鼠胃底黏膜制备功能良好的ECL细胞制剂(纯度约80%)。细胞在0.1 nM胃泌素存在的情况下培养48小时;然后洗涤细胞,并单独与拮抗剂或与不同浓度的拮抗剂加10 nM胃泌素(最大有效浓度)一起孵育30分钟。在不存在或存在浓度递增的拮抗剂的情况下构建胃泌素剂量-反应曲线。通过放射免疫测定法测定分泌的胰抑制素量。4. 胃泌素诱发的胰抑制素分泌呈剂量依赖性受到抑制。YM022、AG041R和YF476的IC50值分别为0.5、2.2和2.7 nM。L-740,093、JB93182和RP73870的IC50值为7.8、9.3和9.8 nM,而PD135158、PD136450和PD134308的IC50值为76、135和145 nM。CCK1受体拮抗剂地伐西匹是一种较差的CCK2受体拮抗剂,IC50约为800 nM。5. 选择YM022、YF476和AG041R进行进一步分析。YM022和YF476以提示竞争性拮抗作用的方式使胃泌素剂量-反应曲线右移,而AG041R的作用无法用简单的竞争性拮抗作用来解释。YM022的pK(B)值为11.3,YF476的为10.8,AG041R的表观pK(B)为10.4。

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