Cholinergic dependence of gallbladder response to cholecystokinin in the guinea pig in vivo.
Cholinergic dependence of gallbladder response to cholecystokinin in the guinea pig in vivo.
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豚鼠体内胆囊对胆囊收缩素反应的胆碱能依赖性。
DOI：
10.1152/ajpgi.1991.261.4.g565
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Owyang,C
中科院分区：
文献类型：
--
作者：
Takahashi,T;May,D;Owyang,C
胆囊收缩素（CCK）诱导胆囊（GB）收缩的生理机制尚不清楚。我们研究了在生理和超生理水平的CCK-八肽（CCK-8）的直接肌肉刺激和神经激活的相对作用，在体内豚鼠模型。通过插入GB腔的压力传感器测量GB压力。CCK-8（2.5-40 ng·kg ~（-1）·min ~（-1））可使胆囊收缩压呈剂量依赖性升高。阿托品或六甲双铵预处理可拮抗低剂量CCK-8（2.5-5 ng·kg-1·min-1）引起的GB反应，但对剂量大于10 ng·kg-1·min-1的反应无影响。双侧迷走神经干切断术也显著降低了GB对低剂量CCK-8（2.5-5 ng·kg-1.min-1）的反应，但对高剂量CCK-8（10-40 ng·kg-1.min-1）的反应没有影响。阿托品或六烃季铵对接受迷走神经干切断术的豚鼠没有进一步的抑制作用。自由进食的禁食豚鼠产生的餐后血浆CCK峰值水平为7.8 +/- 1.8 pM。输注5 ng.kg-1.min-1 CCK-8（8.4 +/- 2.6 pM）最接近该水平。CCK-8以大于或等于10 ng·kg ~（-1）·min ~（-1）的剂量输注可产生超生理的血浆CCK水平。这些观察结果表明，CCK刺激通过神经和直接平滑肌效应的GB收缩。产生生理血浆CCK水平的CCK-8剂量通过刺激迷走神经介导途径中的突触前胆碱能神经元起作用，而产生超生理CCK水平的CCK-8剂量直接作用于GB平滑肌。（250字处删节）
The physiological mechanism responsible for cholecystokinin (CCK)-induced gallbladder (GB) contraction is unclear. We investigated the relative roles of direct muscle stimulation and neural activation at physiological and supraphysiological levels of CCK-octapeptide (CCK-8) using an in vivo guinea pig model. GB pressure was measured by a pressure transducer inserted into the GB lumen. Infusion of CCK-8 (2.5-40 ng.kg-1.min-1) increased GB pressure in a dose-dependent fashion. Pretreatment with atropine or hexamethonium antagonized GB responses to low doses of CCK-8 (2.5-5 ng.kg-1.min-1) but had no effect on doses greater than 10 ng.kg-1.min-1. Bilateral truncal vagotomy also significantly reduced GB responses to low doses of CCK-8 (2.5-5 ng.kg-1.min-1) but did not affect responses to high doses (10-40 ng.kg-1.min-1). Atropine or hexamethonium had no further inhibitory effects on guinea pigs that had undergone truncal vagotomy. Fasted guinea pigs that were fed ad libitum produced a postprandial peak plasma CCK level of 7.8 +/- 1.8 pM. This level was most closely approximated by infusion of 5 ng.kg-1.min-1 of CCK-8 (8.4 +/- 2.6 pM). CCK-8 infusion at greater than or equal to 10 ng.kg-1.min-1 gave supraphysiological plasma CCK levels. These observations indicate that CCK stimulated GB contraction via both a neural and a direct smooth muscle effect. Doses of CCK-8 that produce physiological plasma CCK levels act via stimulation of presynaptic cholinergic neurons in a vagally mediated pathway, whereas doses of CCK-8 that produce supraphysiological CCK levels act directly on GB smooth muscle.(ABSTRACT TRUNCATED AT 250 WORDS)
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影响因子：
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作者：
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DOI：
10.1056/nejm198204153061504
发表时间：
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期刊：
The New England journal of medicine
影响因子：
--
作者：
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DOI：
--
发表时间：
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期刊：
The Journal of biological chemistry
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