Yonezawa H
Jpn J Physiol. 1984;34(5):849-56. doi: 10.2170/jjphysiol.34.849.
Injection of various trypsin inhibitors into the lumen of the isolated perfused rat duodenum increased the amount of biologically active cholecystokinin-pancreozymin (CCK-BA) in the vascular perfusate. The potency to induce CCK-BA release of the various trypsin inhibitors differed. Injection of ethyl p-(6-guanidinohexanoyloxy) benzoate methanesulfonate (FOY-007; 100 mumol), p-ethoxy-carbamoyl-thio-6-guanidino caproate phosphate (FOY-129; 110 mumol), 4-(4-guanidino-benzoyloxy) phenylacetic acid (FOY-251; 128 mumol), N,N-dimethyl-carbamoylmethyl-4-(4-guanidinobenzoyloxy) phenylacetate methanesulfonate (FOY-305; 80 mumol), and p-aminobenzamidine dihydrochloride (p-ABA, Sigma; 300 mumol) caused release of CCK-BA amounting to 1,042, 247, 252, 682, and 302 pM, respectively. The potency to induce CCK-BA release was not correlated with the potency to inhibit trypsin activity. The present results do not support the hypothesis that a negative feed-back regulation of pancreatic enzyme secretion is exerted by intraluminal trypsin in the rat.
将各种胰蛋白酶抑制剂注入离体灌流的大鼠十二指肠肠腔，可增加血管灌流液中生物活性胆囊收缩素-促胰酶素（CCK-BA）的含量。不同胰蛋白酶抑制剂诱导CCK-BA释放的能力有所不同。注射对（6-胍基己酰氧基）苯甲酸乙酯甲磺酸盐（FOY-007；100 μmol）、对乙氧基甲酰硫基-6-胍基己酸磷酸盐（FOY-129；110 μmol）、4-（4-胍基苯甲酰氧基）苯乙酸（FOY-251；128 μmol）、N，N-二甲基氨甲酰甲基-4-（4-胍基苯甲酰氧基）苯乙酸甲磺酸盐（FOY-305；80 μmol）和对氨基苯甲脒二盐酸盐（p-ABA，Sigma；300 μmol）分别导致CCK-BA释放量达到1042、247、252、682和302 pM。诱导CCK-BA释放的能力与抑制胰蛋白酶活性的能力无关。目前的结果不支持大鼠肠腔内胰蛋白酶对胰腺酶分泌进行负反馈调节这一假说。
