Cholecystokinin at physiological levels evokes pancreatic enzyme secretion via a cholinergic pathway.
Cholecystokinin at physiological levels evokes pancreatic enzyme secretion via a cholinergic pathway.
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生理水平的胆囊收缩素通过胆碱能途径引起胰酶分泌。
DOI：
10.1152/ajpgi.1992.263.1.g102
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Owyang,C
中科院分区：
文献类型：
--
作者：
Soudah,HC;Lu,Y;Hasler,WL;Owyang,C
研究了生理浓度的胆囊收缩素（CCK）引起人胰腺外分泌的机制。八肽胆囊收缩素（CCK-8）剂量依赖性地增加胰蛋白酶和脂肪酶的输出在健康人。阿托品抑制CCK-8（10 ng.kg-1. h-1）刺激的胰蛋白酶分泌84.0 +/- 7.7%，脂肪酶分泌78.6 +/-9.2%。CCK-8剂量为40 ng.kg-1. h-1时，阿托品的抑制作用要小得多（胰蛋白酶为41.8 +/- 6.6%，脂肪酶为46.3 +/- 7.3%）。CCK-8在10 ng.kg-1.h-1剂量下产生的血浆CCK水平与餐后水平相似（6.0 +/- 1.3 pM vs. 6.9 +/- 0.8 pM），而40 ng.kg-1.h-1剂量产生的水平高于生理水平（18.4 +/- 3.1 pM）。为了评估CCK是否可能通过刺激胆碱能神经起作用，使用大鼠胰腺进行了体外研究。CCK-8（10 nM-10 μ M）刺激胰腺小叶释放[3 H]乙酰胆碱，而这种释放被河豚毒素（一种无钙培养基）和CCK拮抗剂L364，718阻断。总之，CCK刺激的胰腺酶分泌依赖于胆碱能神经和非胆碱能途径。在人类中，CCK输注产生的血浆CCK水平与餐后观察到的水平相似，主要通过依赖于胆碱能神经支配的途径刺激胰腺。相关的体外实验表明，CCK可能通过刺激神经乙酰胆碱的释放而发挥作用。相比之下，超生理CCK输注部分通过非胆碱能途径起作用。
The mechanism by which physiological concentrations of cholecystokinin (CCK) evoke pancreatic exocrine secretion in humans was investigated. CCK octapeptide (CCK-8) dose dependently increased trypsin and lipase output in healthy humans. Atropine inhibited CCK-8 (10 ng.kg-1.h-1)-stimulated trypsin output by 84.0 +/- 7.7% and lipase output by 78.6 +/- 9.2%. The inhibition with atropine was much less with a CCK-8 dose of 40 ng.kg-1.h-1 (41.8 +/- 6.6% for trypsin and 46.3 +/- 7.3% for lipase). CCK-8 at 10 ng.kg-1.h-1 produced plasma CCK levels similar to postprandial levels (6.0 +/- 1.3 vs. 6.9 +/- 0.8 pM), whereas the 40-ng.kg-1.h-1 dose produced supraphysiological levels (18.4 +/- 3.1 pM). To evaluate if CCK might act via stimulation of cholinergic nerves, in vitro studies were performed using rat pancreas. CCK-8 (10 nM-10 microM) stimulated [3H]acetylcholine release from pancreatic lobules that was blocked by tetrodotoxin, a calcium-free medium, and the CCK antagonist L364,718. In conclusion, CCK-stimulated pancreatic enzyme secretion is dependent on cholinergic neural and noncholinergic pathways. In humans, CCK infusions, which produce plasma CCK levels similar to those seen postprandially, stimulate the pancreas predominantly via a pathway dependent on cholinergic innervation. Correlative in vitro experiments suggest that CCK may act by stimulation of neural acetylcholine release. In contrast, supraphysiological CCK infusions act in part via noncholinergic pathways.