Vagal control of migrating motor complex-related peaks in canine plasma motilin, pancreatic polypeptide, and gastrin.

The role of the vagus nerve in the control of fasting plasma pancreatic polypeptide (PP), gastrin, and motilin levels was investigated in conscious dogs. Lowest plasma levels of motilin (81 +/- 8 pmol/L), PP (19 +/- 1 pmol/L) and gastrin (5 +/- 1 pmol/L) were observed during phase I of the migrating motor complex (MMC). Significant peaks in plasma motilin (127 +/- 11 pmol/L, P less than 0.005), PP (26 +/- 2 pmol/L, P less than 0.005), and gastrin (14 +/- 2 pmol/L, P less than 0.005) were seen, coinciding with the appearance of phase II (PP and gastrin) or phase III (motilin) of the migrating motor complex in the upper gut. Whereas bilateral vagal blockade abolished the peaks in PP and gastrin, a significant (P less than 0.025) increment in plasma motilin remained, which correlated with the late phase III equivalent of the vagally independent complex (VIC) in the duodenum. This VIC-related motilin peak (170 +/- 20 pmol/L) was significantly higher (P less than 0.025) and the time course (9 +/- 2 min) significantly shorter (P less than 0.01) than the peak (127 +/- 11 pmol/L) and duration (31 +/- 9 min) observed without vagal blockade. Thus, in fasting, the cyclical increments of PP and gastrin are both dependent on excitatory vagal innervation, whereas excitatory pathways controlling phase III associated peak motilin release are nonvagal. In addition, the pattern of fasting motilin release and the amplitude of peak motilin secretion may be affected by vagal inhibition.