Martinez V, Jimenez M, Goñalons E, Vergara P
Department of Cell Biology and Physiology, Veterinary Faculty, Universitat Autonoma de Barcelona, Bellaterra, Spain.
Am J Physiol. 1993 Nov;265(5 Pt 1):G842-50. doi: 10.1152/ajpgi.1993.265.5.G842.
Our objective was to study the mechanism of action of cholecystokinin (CCK) on the motility of the gastroduodenal area. Chickens were implanted with five electrodes for electromyography in the stomach and duodenum. The effects of CCK (10(-9) mol.kg-1.10 min-1) were studied against the presence of several antagonists and in vagotomized animals. CCK caused inhibition of gastric motility and duodenal hyperactivity. Vagotomy blocked CCK responses in the stomach but not in the duodenum. Hexamethonium partially blocked gastric inhibition induced by CCK. NG-nitro-L-arginine methyl ester blocked the inhibitory response to CCK in the stomach but did not modify duodenum response. L-Arginine did not modify CCK actions. Opioid antagonists naloxone and naltrindole and adrenergic antagonists phentolamine and propranolol did not modify CCK response. Atropine did not modify duodenal response to CCK. Sodium nitroprusside (10(-8)-10(-6) mol/kg) inhibited gastroduodenal activity in a dose-related manner. We suggest that gastric response to CCK is vagally mediated, mainly by the nitric oxide system. Duodenal hyperactivity seems to be a direct action of CCK. Nitric oxide is a putative neurotransmitter in the chicken gut.
我们的目的是研究胆囊收缩素（CCK）对胃十二指肠区域运动的作用机制。将五只电极植入鸡的胃和十二指肠用于肌电图检查。研究了CCK（10⁻⁹摩尔·千克⁻¹·10分钟⁻¹）在几种拮抗剂存在的情况下以及在迷走神经切断动物中的作用。CCK导致胃运动抑制和十二指肠活动亢进。迷走神经切断术阻断了胃对CCK的反应，但未阻断十二指肠的反应。六甲铵部分阻断了CCK诱导的胃抑制。NG-硝基-L-精氨酸甲酯阻断了胃对CCK的抑制反应，但未改变十二指肠的反应。L-精氨酸未改变CCK的作用。阿片类拮抗剂纳洛酮和纳曲吲哚以及肾上腺素能拮抗剂酚妥拉明和普萘洛尔未改变CCK的反应。阿托品未改变十二指肠对CCK的反应。硝普钠（10⁻⁸ - 10⁻⁶摩尔/千克）以剂量相关的方式抑制胃十二指肠活动。我们认为胃对CCK的反应是由迷走神经介导的，主要通过一氧化氮系统。十二指肠活动亢进似乎是CCK的直接作用。一氧化氮是鸡肠道中一种假定的神经递质。
