Okubo K, Miyasaka K, Matsumoto M, Funakoshi A
Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology, Japan.
Pancreas. 1994 Sep;9(5):585-90. doi: 10.1097/00006676-199409000-00008.
The mechanisms of the stimulatory effect of the bombesin-like peptide neuromedin C on pancreatic exocrine secretion were examined in conscious rats. Rats were prepared with cannulae draining bile and pancreatic juice separately. Intravenous infusion of 0.35 nmol/kg/h of neuromedin C significantly increased the secretions of pancreatic bicarbonate and protein, and transiently increased the plasma cholecystokinin (CCK) concentration. The increase in pancreatic secretion persisted for 90 min, whereas the increase in plasma CCK was observed only after 15 and 30 min from the beginning of neuromedin C infusion. Intravenous infusion of CR-1409, a specific CCK-receptor antagonist, inhibited, but did not abolish, the protein secretion stimulated by neuromedin C. Intraduodenal infusion of a potent proton pump inhibitor, omeprazole, suppressed, but did not abolish, protein secretion induced by neuromedin C. Omeprazole abolished the increase in bicarbonate secretion produced by neuromedin C. These results indicate that neuromedin C induces release of CCK and that its induction of pancreatic hypersecretion is due to both its direct effect and CCK. The results also suggest that gastric hypersecretion may have a role in the bicarbonate hypersecretion induced by neuromedin C.
在清醒大鼠中研究了蛙皮素样肽神经介素C对胰腺外分泌的刺激作用机制。通过插管分别引流胆汁和胰液来制备大鼠。静脉输注0.35 nmol/kg/h的神经介素C显著增加了胰腺碳酸氢盐和蛋白质的分泌，并短暂提高了血浆胆囊收缩素（CCK）浓度。胰腺分泌的增加持续了90分钟，而血浆CCK的增加仅在神经介素C输注开始后的15分钟和30分钟后观察到。静脉输注特异性CCK受体拮抗剂CR-1409可抑制但不能消除神经介素C刺激的蛋白质分泌。十二指肠内输注强效质子泵抑制剂奥美拉唑可抑制但不能消除神经介素C诱导的蛋白质分泌。奥美拉唑消除了神经介素C引起的碳酸氢盐分泌增加。这些结果表明，神经介素C诱导CCK释放，其诱导胰腺分泌亢进是由于其直接作用和CCK共同作用。结果还表明，胃酸分泌过多可能在神经介素C诱导的碳酸氢盐分泌过多中起作用。
