Adachi H, Toda N, Hayashi S, Noguchi M, Suzuki T, Torizuka K, Yajima H, Koyama K
Gastroenterology. 1981 Apr;80(4):783-8.
Synthetic motilin caused a dose-dependent contraction on isolated rabbit intestinal segments, including the duodenum, ileum, and rectum. The contraction of duodenum was significantly greater than that in the ileum or rectum. In the duodenum, motilin was approximately 100 times as potent as acetylcholine on molar basis. The motilin-induced contractions were not influenced by atropine, chlorpheniramine, cimetidine, phentolamine, propranolol, cinanserin, 1-sar-8-ala-angiotensin II, or aspirin. Motilin did not affect the contraction induced by transmural electrical stimulation or acetylcholine. The response to motilin was unaffected by acetylcholine. Removal of Ca++ from bathing media or verapamil suppressed the motilin-induced contractions to a significantly greater extent than the contractions induced by acetylcholine. Thus, it may be concluded that motilin produces intestinal contractions by acting directly on smooth muscles, but not by acting on pharmacologically known drug receptors nor by releasing neurotransmitters such as endogenous acetylcholine. Motilin does not appear to modify autonomic nerve functions.
合成胃动素对离体兔肠段（包括十二指肠、回肠和直肠）产生剂量依赖性收缩作用。十二指肠的收缩明显大于回肠或直肠。在十二指肠，按摩尔计算，胃动素的效力约为乙酰胆碱的100倍。胃动素诱导的收缩不受阿托品、氯苯那敏、西咪替丁、酚妥拉明、普萘洛尔、辛那色林、1-肌氨酸-8-丙氨酸血管紧张素II或阿司匹林的影响。胃动素不影响经壁电刺激或乙酰胆碱诱导的收缩。对胃动素的反应不受乙酰胆碱的影响。从浴液中去除Ca++或维拉帕米对胃动素诱导的收缩的抑制程度明显大于对乙酰胆碱诱导的收缩的抑制程度。因此，可以得出结论，胃动素通过直接作用于平滑肌产生肠道收缩，而不是通过作用于药理学上已知的药物受体，也不是通过释放内源性乙酰胆碱等神经递质。胃动素似乎不改变自主神经功能。
