Respective roles of CCK-A and B receptors in the regulation of pancreatic secretion

在人类中， CCK已经被已知通过CCK-A受体刺激泛氮酶的秘密。毫无疑问，最近有报道称，通过Northen blot分析，CCK的基因表达--人类阴茎中的受体可能无法检测到。在目前的研究中，我们审查了CCK对人类阴茎的调节机制，并将老鼠和老鼠中的老鼠进行了比较。任何CCK都不能从人类阴茎感染者的抗生素、GRP和乙酰舒氨酸中刺激淀粉酶释放。由乙酰胆碱素和GRP拮抗剂抑制的淀粉酶释放，尊重地。CCK-A受体基因表达没有通过北方印迹分析检测到，但CCK-B受体基因表达在人类胰腺中检测到。Autoradiography using a D1125-CCK-8 revealed positive binding sites in the human pancreas and these bindings were replaced by a CCK-B receptor antagonist but not by a CCK-A receptor antagonist。D1125 D1-CCK-8 also bound human duo ... More 拒绝和被CCK取代-一个受体拮抗剂。因此，我们确认CCK-B受体，而不是A受体，在人类的阴茎中是丰富的，而且CCK并没有从急性细胞中刺激淀粉酶释放，直接。在老鼠中，蒸汽中的血管效应神经对CCK负责，而兴奋被CCK-A受体拮抗剂阻断，而不是B受体拮抗剂阻断。结合在一起，这就解释了CCK刺激的人类阴茎通过血管紧张的神经，并通过血管复合体（血管-血管反射）通过血管紧张的复合体。在CCD-B受体基因knockout老鼠中测试了婴儿和阴道果汁的秘密。CCK-B受体的缺陷并没有改变这些秘密，或过度增长。因此， CCK-B受体不是婴儿和泛闭性保密或其他规定可能补偿CCK-B受体功能的强制性。CCK-一个接受者基因敲出老鼠已经生成了。他们显示出正常的增长，而且很容易。“婴儿和泛大麻果汁的秘密没有被CCK刺激，但对其他刺激者（如GRP和乙酰胆碱）有反应。”“肥胖的湿重在三种基因上并不不同。”在老鼠，CCK-一个接受者基因表达已经被知道在出生后出现。我们报告了这个基因表达与死亡有关的问题。Less（低）

In humans, CCK has been known to stimulate pancreatic enzyme secretion via CCK-A receptors. Nevertheless, it was recently reported that gene expression of CCK-A receptor in the human pancreas could not be detected by Northen blot analysis. In the present study, we examined the mechanism of regulation of human pancreas by CCK and compared with those in mice and rats.Any dose of CCK could not stimulate amylase release from the human pancreatic dispersed acini, whereas GRP and acetylsholine did. The amylase release stimulated by acetylcholein and GRP were inhibited by atropine and a GRP antagonist, respectively. CCK-A receptor gene expression was not detected by Northern blot analysis but CCK-B receptor gene expression was detected in the human pancreas. Autoradiography using aィイD1125ィエD1-CCK-8 revealed positive binding sites in the human pancreas and these bindings were replaced by a CCK-B receptor antagonist but not by a CCK-A receptor antagonist. 1ィイD1125ィエD1-CCK-8 also bound human duo … More denum and was replaced by CCK-A receptor antagonist. Therefore, we confirmed that CCK-B receptors, not A receptors, were rich in human pancreas and that CCK did not stimulate amylase release from the acinar cells, directly.In rats, vagal afferent nerves in the stomach was responsible for CCK and the excitation was blocked by CCK-A receptor antagonist, not by B receptor antagonist. Taken together, it is interpreted that CCK stimulated human pancreas via vagal afferent nerve and passing through the vagal complex in the brain (vago-vagal reflex).The bile and pancreatic juice secretion were examined in CCD-B receptor gene knockout mice. The lack of CCK-B receptor did not modify these secretions, or pancreatic growth. Thus, CCK-B receptor is not mandatory for the bile and pancreatic secretion or other regulation may compensate CCK-B receptor function. The CCK-A receptor gene knockout mice have been generated. They shows normal growth and are fertile. The bile and pancreatic juice secretion were not stimulated by CCK but were responsible for other stimulants such as GRP and acetylcholine. The pancreatic wet weight was not different among three genotypes. In rats, CCK-A receptor gene expression has been known to appear after birth. We reported this gene expression was correlated with demthylation. Less