Kanno T, Saito A
Endocrinol Jpn. 1980 Dec;27 Suppl 1:51-7. doi: 10.1507/endocrj1954.27.supplement_51.
Secretory actions of VIP (vasoactive intestinal peptide), secretin and CCK-PZ (Cholecystokinin-pancreozymin) were compared in the isolated and perfused kitten pancreas. Perfusion of the isolated kitten pancreas with a solution containing 20 mU/ml CCK-PZ resulted in gradual hyperpolarization of the pancreatic acinar cell. CCK-PZ induced a dose-dependent increase in the pancreatic protein output and a small but definite increase in the flow of pancreatic juice which was also dose dependent upon CCK-PZ. Secretin and VIP induced a dose-dependent increase in the flow but a negligible increase in the pancreatic protein output. The estimated ED50 for VIP was 1.5 nM which was 5 times as large as the estimated ED50 for secretin. A considerable amount of VIP, which corresponded roughly to the activity of exogenous 0.6 nM VIP, was spontaneously released from the isolated kitten duodenum into the portal vein, and this VIP release was nullified during vascular perfusion with a Ca-deficient solution. With respect to these and other results, we will propose a view concerning a possible role of VIP in controlling the function of the exocrine pancreas.
在离体灌注的幼猫胰腺中，对血管活性肠肽（VIP）、促胰液素和缩胆囊素-促胰酶素（CCK-PZ）的分泌作用进行了比较。用含20 mU/ml CCK-PZ的溶液灌注离体幼猫胰腺，会导致胰腺腺泡细胞逐渐发生超极化。CCK-PZ可使胰腺蛋白质分泌量呈剂量依赖性增加，胰液分泌量虽有少量但明显增加，且同样呈CCK-PZ剂量依赖性。促胰液素和VIP可使胰液分泌量呈剂量依赖性增加，但胰腺蛋白质分泌量增加可忽略不计。VIP的估计半数有效剂量（ED50）为1.5 nM，是促胰液素估计ED50的5倍。相当数量的VIP（大致相当于外源性0.6 nM VIP的活性）从离体幼猫十二指肠自发释放到门静脉中，在用缺钙溶液进行血管灌注时，这种VIP释放被消除。关于这些及其他结果，我们将提出一个关于VIP在控制外分泌胰腺功能中可能作用的观点。
