Gene expressions of the cholecystokinin (CCK) and CCK receptors, and regulation of pancreatic exocrine function

1.胰管结扎（PL）引起的血浆CCK水平升高，使CCK mRNA和PSTI-61 mRNA表达增加，分别在PL后第10天和第3天达到最高，CCK-A受体mRNA表达下降，第7天达到最低，第10天和第3天达到最高，第10天和第3天达到最低。从肠中排除胆胰液（BPJ）也产生高血浆CCK水平，CCK受体拮抗剂可抑制CCK mRNA和PSTI-61 mRNA的表达，而CCK类似物可使CCK mRNA和PSTI-61 mRNA的表达增加。在腹部手术后4-5天内，分别于BPJ转流后1、2、4、24小时检测CCK、促胰液素和PSTI-61的mRNA水平，结果表明，BPJ转流后CCK、促胰液素和PSTI-61的mRNA水平均明显高于BPJ转流后CCK、促胰液素和PSTI-61的mRNA水平。胰腺炎相关蛋白（PAP）基因表达消失，CCK和促胰液素mRNA表达增加，而PSTI-61 mRNA表达无明显变化。3.老年雄性大鼠CCK和CCK-A、B受体mRNA表达降低，而雌性大鼠CCK和CCK-A、B受体mRNA表达无明显变化，迷走神经传出神经的参与对CCK刺激的胰腺外分泌的调节作用比传入神经的作用更重要，中枢给予生长抑素抑制胰腺分泌可通过交感神经引起BPJ分流。

1.The purification of CCK-Releasing Peptide (CCK-RP) is in progress.2.The high plasma CCK levels produced by pancreatic duct ligation (PL) increased CCK mRNA and PSTI-61 mRNA,and the maximal levels were observed on day 10 and 3 after PL,respectively.The CCK-A receptor mRNA decreased and reached the nadir on day 7, then recovered.Exclusion of bile-pancreatic juice (BPJ) from the intestine also produced the high plasma CCK level, and increased CCK mRNA and PSTI-61 mRNA levels.Administration of CCK antagonist reduced these increases.Administration of CCK analogue increased both CCK and PSTI-61 mRNA levels, however the increases were less that those produced by BPJ diversion.Therefore, it is suggested that not only CCK but also other factors may be involved in these regulations.When the levels of CCK,secretin and PSTI-61 mRNAs were examined 1,2,4,24 hours after BPJ diversion during 4-5 days after abdominal surgery, during which the gene expression of pancreatitis associated protein (PAP) was disappeared, the mRNA levels of CCK and secretin increased but not that of PSTI-61 mRNA.3.The levels of CCK and CCK-A,B receptor mRNAs decreased in old male rats, but not in female rats, and the changes in these mRNA levels in the intestine and the brain associated with age were variable.4.The involvement of vagal efferent nerve was more important to regulate CCK-stimulated pancreatic exocrine secretion, compared with afferent nerve function.The central administration of somatostatin inhibited pancreatic secretion produced BPJ diversion via synpathetic nerve.