Modulation of gallbladder motility by intrinsic cholinergic neurons.
Modulation of gallbladder motility by intrinsic cholinergic neurons.
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内在胆碱能神经元调节胆囊运动。
DOI：
10.1152/ajpgi.1984.247.6.g662
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Youther,ML
中科院分区：
文献类型：
--
作者：
Yau,WM;Youther,ML
通过使用经受透壁场刺激的离体豚鼠胆囊制剂来研究乙酰胆碱（ACh）的机械收缩和释放。研究发现收缩幅度的增加与施加刺激的频率（5-60 Hz）有关。用河豚毒素和阿托品治疗可以防止这些电引起的收缩。电刺激或盐酸藜芦碱去极化可同时增加乙酰胆碱的释放，并且这种增加容易被河豚毒素阻断。 0.1 Hz 的刺激无法检测到收缩和乙酰胆碱释放。当对由超最大浓度的胆囊收缩素八肽（CCK-8）诱导的收缩胆囊进行场刺激时，观察到肌张力进一步增加。这种增加的幅度取决于频率。尽管对场透壁刺激的反应开始相对较快，但获得的最大反应仅为CCK-8引起的反应的70%。当组织暴露于2.2 X 10(-6) M CCK-8时，肌肉收缩最大，但[3H]ACh的流出没有增加。这些数据提供了内在胆囊胆碱能神经元的药理学特征，并证明了它们在控制胆囊运动中可能发挥的可能作用。
The mechanical contraction and release of acetylcholine (ACh) were investigated by use of an isolated guinea pig gallbladder preparation subjected to transmural field stimulation. An increase in contraction amplitude was found to be related to the frequency (5-60 Hz) of applied stimulus. Treatment with tetrodotoxin and atropine prevented these electrically induced contractions. A simultaneous increase in the release of ACh was noted with electrical stimulation or depolarization by veratrine hydrochloride, and this increase was susceptible to blockade by tetrodotoxin. Neither contractions nor ACh release could be detected with stimulation at 0.1 Hz. When field stimulation was applied to contracted gallbladder induced by a supramaximal concentration of cholecystokinin octapeptide (CCK-8), a further increase in muscle tone was observed. The magnitude of this increase was frequency dependent. Although the onset of response to field transmural stimulation was relatively more rapid, the maximal response attained was only 70% of that elicited by CCK-8. When tissues were exposed to 2.2 X 10(-6) M CCK-8, the muscle contracted maximally but there was no increase in the efflux of [3H]ACh. These data provide a pharmacological characterization of the intrinsic gallbladder cholinergic neurons and demonstrate a possible role they may play in the control of gallbladder motility.