Schwartz G J, Moran T H, White W O, Ladenheim E E
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205-2196, USA.
Am J Physiol. 1997 Jun;272(6 Pt 2):R1726-33. doi: 10.1152/ajpregu.1997.272.6.R1726.
The brain-gut peptides cholecystokinin (CCK) and the mammalian bombesin-like peptide gastrin-releasing peptide (GRP) suppress food intake. Vagotomy blocks CCK- but not bombesin (BN)-induced feeding suppression, demonstrating differential vagal contributions. We examined the relationship between the ability of CCK and the active fragment of GRP, GRP-(18-27), to stimulate gastric vagal afferent activity and their ability to elicit changes in gastric motility. We also examined ligated cervical vagal segments and revealed specific 125I-CCK vagal binding without evidence of radiolabeled BN binding sites. Both close arterial and intraperitoneal CCK and GRP-(18-27) produced dose-dependent increases in activity in gastric vagal mechanoreceptive afferents. CCK dose dependently decreased gastric pressure without altering antral wall tension, whereas GRP-(18-27) dose dependently increased both gastric pressure and peak antral wall muscle tension. These results suggest that GRP-(18-27) activates gastric vagal afferents secondary to its stimulation of gastric motor effects. CCK activates this same population of vagal afferents independent of changes in gastric tension, suggesting a direct action of CCK at functional vagal CCK receptors.
脑肠肽胆囊收缩素（CCK）和哺乳动物促胃液素释放肽（GRP）样蛙皮素可抑制食物摄入。迷走神经切断术可阻断CCK诱导的摄食抑制，但不能阻断蛙皮素（BN）诱导的摄食抑制，这表明迷走神经的作用存在差异。我们研究了CCK和GRP活性片段GRP-(18-27)刺激胃迷走神经传入活动的能力与其引起胃动力变化的能力之间的关系。我们还检查了结扎的颈迷走神经节段，发现有特异性的125I-CCK迷走神经结合，但没有放射性标记的BN结合位点的证据。动脉内和腹腔内注射CCK和GRP-(18-27)均可使胃迷走机械感受性传入神经的活动呈剂量依赖性增加。CCK剂量依赖性地降低胃内压，而不改变胃窦壁张力，而GRP-(18-27)剂量依赖性地增加胃内压和胃窦壁肌肉张力峰值。这些结果表明，GRP-(18-27)通过刺激胃运动效应而继发激活胃迷走神经传入神经。CCK独立于胃张力变化激活同一群迷走神经传入神经，提示CCK在功能性迷走神经CCK受体上有直接作用。
