Intracerebroventricular injection of somatostatin sst5 receptor agonist inhibits gastric acid secretion in rats.
Intracerebroventricular injection of somatostatin sst5 receptor agonist inhibits gastric acid secretion in rats.
复制标题
脑室内注射生长抑素sst5受体激动剂抑制大鼠胃酸分泌。
DOI：
10.1016/0014-2999(95)00690-7
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Tache,Y
中科院分区：
文献类型：
--
作者：
Martinez,V;Coy,DH;Lloyd,KC;Tache,Y
生长抑素及其类似物在大脑中作用，影响胃酸分泌。已鉴定出五种不同的生长抑素受体亚型（sst1 至 sst5）。我们研究了生长抑素（0.18-0.6 nmol/大鼠）和选择性 sst2、sst3 和 sst5 受体配体对配备慢性胃插管和脑室插管的清醒大鼠基础胃酸分泌的影响。生长抑素-14 (0.36 nmol/大鼠)、sst2、sst3 和 sst5 受体激动剂、Des-AA1,2,4,5,12,13-[d-Tryp8,d-Cys14]生长抑素 (SMS 201–995) (0.18–0.36 nmol/大鼠) 和 sst5 受体激动剂， BIM-23052，（0.8–1.2 nmol/大鼠）静脉注射抑制胃酸分泌。生长抑素-14 (0.36 nmol/大鼠)、SMS 201-995 (0.18 nmol/大鼠) 和 BIM-23052 (0.8 nmol/大鼠) 分别诱导最大抑制达到 42%、60% 和 42%。 sst2 受体激动剂 DC 32-87（0.2-0.8 nmol/大鼠）和 sst3 受体激动剂 BIM-23056（0.2-1.2 nmol/大鼠）不会改变胃酸分泌，但 0.4 nmol/大鼠的 sst3 受体激动剂会增加注射后 20 分钟的酸排出量。 sst2受体激动剂（0.4 nmol/大鼠）与阈下剂量的sst5（0.4 nmol/大鼠）共同静脉注射抑制胃酸分泌。这些结果表明 i.c.v.注射生长抑素-14 通过对 sst5 受体亚型的作用抑制清醒大鼠的基础胃酸分泌，该作用可通过 sst2 受体亚型增强。
Somatostatin and its analogs act in the brain to influence gastric acid secretion. Five different somatostatin receptor subtypes have been characterized (sst1to sst5). We studied the influence of somatostatin (0.18–0.6 nmol/rat) and selective sst2, sst3and sst5receptor ligands on basal gastric acid secretion in conscious rats equipped with chronic gastric and intracerebroventricular (i.c.v.) cannulae. Somatostatin-14 (0.36 nmol/rat), the sst2, sst3and sst5receptor agonist, Des-AA1,2,4,5,12,13-[d-Tryp8,d-Cys14]somatostatin (SMS 201–995) (0.18–0.36 nmol/rat) and the sst5receptor agonist, BIM-23052, (0.8–1.2 nmol/rat) injected i.c.v. inhibited gastric acid secretion. Maximal inhibition reaching 42%, 60% and 42% was induced by somatostatin-14 (0.36 nmol/rat), SMS 201–995 (0.18 nmol/rat) and BIM-23052 (0.8 nmol/rat) respectively. The sst2receptor agonist, DC 32–87 (0.2–0.8 nmol/rat) and sst3receptor agonist, BIM-23056 (0.2–1.2 nmol/rat), did not modify gastric acid secretion, except the sst3receptor agonist at 0.4 nmol/rat which increased acid output at 20 min post-injection. The sst2receptor agonists (0.4 nmol/rat) co-injected i.c.v with a subthreshold dose of sst5(0.4 nmol/rat) inhibited gastric acid secretion. These results show that i.c.v. injection of somatostatin-14 inhibits basal gastric acid secretion in conscious rats through an action on sst5receptor subtype which can be potentiated by sst2receptor subtype.