Schwartz G J, McHugh P R, Moran T H
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Am J Physiol. 1994 Jul;267(1 Pt 2):R303-8. doi: 10.1152/ajpregu.1994.267.1.R303.
To identify the transduction mechanisms underlying gastric vagal afferent responses to gastric loads and cholecystokinin (CCK), we investigated the ability of specific CCK antagonists, acute pylorectomy, and cholinergic blockade to effect these vagal afferent responses. The CCK-B antagonist L-365,260 (10 pmol-1 nmol) failed to block the gastric vagal afferent response to gastric loads or 100 pmol CCK, while the CCK-A antagonist devazepide (100 pmol-100 nmol) competitively and dose dependently attenuated the response to CCK but not to gastric loads. Application of 100 nmol of the low-affinity CCK receptor antagonist CCK-JMV-180 also completely blocked the gastric vagal afferent response to 100 pmol CCK. Acute pylorectomy failed to block the gastric vagal afferent response to 100 pmol CCK or 2-ml gastric loads. Atropine sulfate administration (15 mg/rat) failed to block the gastric vagal afferent response to 100 pmol CCK or 2-ml gastric loads. These data suggest that 1) the vagal afferent response to CCK is mediated through CCK's interactions with vagal, rather than pyloric, CCK-A receptors, and 2) the vagal afferent responses to CCK and to gastric loads are mediated by dissociable, possibly independent, transduction mechanisms.
为了确定胃迷走神经传入纤维对胃扩张和胆囊收缩素（CCK）反应的转导机制，我们研究了特异性CCK拮抗剂、急性幽门切除术和胆碱能阻断对这些迷走神经传入反应的影响。CCK-B拮抗剂L-365,260（10 pmol - 1 nmol）未能阻断胃迷走神经传入纤维对胃扩张或100 pmol CCK的反应，而CCK-A拮抗剂devazepide（100 pmol - 100 nmol）竞争性地且剂量依赖性地减弱了对CCK的反应，但对胃扩张无影响。应用100 nmol低亲和力CCK受体拮抗剂CCK-JMV-180也完全阻断了胃迷走神经传入纤维对100 pmol CCK的反应。急性幽门切除术未能阻断胃迷走神经传入纤维对100 pmol CCK或2 ml胃扩张的反应。给予硫酸阿托品（15 mg/大鼠）未能阻断胃迷走神经传入纤维对100 pmol CCK或2 ml胃扩张的反应。这些数据表明：1）迷走神经传入纤维对CCK的反应是通过CCK与迷走神经而非幽门CCK-A受体的相互作用介导的；2）迷走神经传入纤维对CCK和胃扩张的反应是由可分离的、可能独立的转导机制介导的。
