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

1983 ◽  
Vol 61 (11) ◽  
pp. 1289-1298 ◽  
Author(s):  
K. E. Hall ◽  
G. R. Greenberg ◽  
T. Y. El-Sharkawy ◽  
N. E. Diamant

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 < 0.005), PP (26 ± 2 pmol/L, P < 0.005), and gastrin (14 ± 2 pmol/L, P < 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 < 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 < 0.025) and the time course (9 ± 2 min) significantly shorter (P < 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.

1983 ◽  
Vol 245 (2) ◽  
pp. G178-G185 ◽  
Author(s):  
K. E. Hall ◽  
N. E. Diamant ◽  
T. Y. El-Sharkawy ◽  
G. R. Greenberg

A potential role of pancreatic polypeptide (PP) in the regulation of phase III of the migrating motor complex (MMC) was investigated in conscious dogs before and during bilateral vagal blockade. After a control fasting period, cyclical increments in plasma PP occurred with peak levels of 45 +/- 8 pmol/l coinciding with late phase II MMC motility. By contrast, after food a substantially higher (approximately five times peak fasting concentrations) and more prolonged elevation of PP was observed, in association with a postprandial pattern of activity. To approximate fasting plasma PP concentrations, porcine PP was infused at 100 pmol X kg-1 X h-1, which produced levels of plasma PP of 99 +/- 8 pmol/l. At this dose PP had no effect on phase III activity. However, at a dose of 400 pmol X kg-1 X h-1, which achieved plasma PP concentrations (283 +/- 33 pmol/l) similar to postprandial levels, there was a specific inhibition of phase III in the lower esophageal sphincter, stomach, duodenum, and upper jejunum. The phase III-associated increment of plasma motilin was also inhibited by this dose of PP. These inhibitory effects at the 400 pmol X kg-1 X h-1 dose of PP were also observed after bilateral blockade of the vagus nerves. Our results suggest that PP has no significant role in the modulation of phase III of the fasting MMC nor does it induce a typical feeding motor pattern. The selective inhibition of both phase III and the associated rise in plasma motilin by PP plasma levels similar to postprandial concentrations does, however, point to a possible role for pancreatic polypeptide in the postprandial inhibition of phase III of the MMC.


1981 ◽  
Vol 59 (2) ◽  
pp. 180-187 ◽  
Author(s):  
J. E. T. Fox ◽  
N. S. Track ◽  
E. E. Daniel

Plasma motilin concentrations were measured in dogs following duodenal acidification and alkalinization and gastric instillation of fat. Antral and duodenal motility were recorded concurrently using intraluminal manometry. Alkalinization of the duodenum produced an increase in antral and duodenal motility and a significant rise in plasma motilin. Alkaline infusions at 5 mL/min into the duodenum initiated phase III of a migrating motor complex both in the antrum and in the duodenum. Duodenal acid infusions produced no change in plasma motilin concentrations while inhibiting antral motility and stimulating duodenal motility for the duration of the infusion. Gastric instillation of 60 g fat produced a 25% increase above basal motilin levels at 50 min after instillation. Motilin levels monitored during spontaneous migrating motor complexes showed peak motilin levels occurring during maximal activity of the antral duodenal region in seven out of nine motor complexes examined but motilin peaks also occurred without migrating complexes being present in this area and, as well, complexes occurred when motilin was undetectable. These results taken together with our other studies in man confirm that a true species difference exists between man and dog in the hormonal motor response to duodenal alkalinization. Although a relationship appears to exist between the appearance of maximal migrating motor complex activity in the gastroduodenal area and plasma motilin concentrations in dogs as in humans, the motilin peaks are probably neither necessary nor sufficient to induce phase III activity.


1987 ◽  
Vol 253 (3) ◽  
pp. G259-G267 ◽  
Author(s):  
H. J. Ehrlein ◽  
M. Schemann ◽  
M. L. Siegle

In the canine small intestine several simple (S) and complex (C) patterns of propulsive and nonpropulsive activities were found. The nonpropulsive activity consisted of 1) stationary individual contractions (S) and 2) stationary clusters of contractions (C). Patterns leading to aboral propulsion of luminal contents were 1) propagating contractions (S), 2) propagating power contractions (S), 3) phase III of the migrating motor complex (C), and 4) migrating clusters of contractions (C). The propagation velocities of the propulsive motor patterns differed markedly; they increased in the following order: phase III, migrating clustered contractions, propagating power contractions, propagating contractions. A retrograde transport of luminal contents was produced by two different activities: 1) retrograde propagating contractions (S) and 2) retrograde power contractions (S). They were accompanied with enterogastric reflux.


1998 ◽  
Vol 114 ◽  
pp. A769
Author(s):  
E. Husebye ◽  
R. Wackerbauer ◽  
J. Bondi ◽  
M. Skard Heier

2000 ◽  
Vol 118 (4) ◽  
pp. A1200
Author(s):  
Toshiyuki Tanaka ◽  
Michael L. Kendrick ◽  
Nicholas J. Zyromski ◽  
Tobias Meile ◽  
Michael G. Sarr

Gut ◽  
1998 ◽  
Vol 42 (1) ◽  
pp. 36-41 ◽  
Author(s):  
J Tack ◽  
B Coulie ◽  
A Wilmer ◽  
T Peeters ◽  
J Janssens

Background—Pharmacological studies of the enteric nervous system have shown the presence of several subtypes of 5-hydroxytryptamine (5HT) receptor, which might be involved in control of the migrating motor complex.Aims—To study the effect of sumatriptan, an agonist of enteric neuronal 5HT1P receptors, on interdigestive motility in man.Subjects and methods—In 12 healthy subjects, interdigestive motility was recorded manometrically in the upper gastrointestinal tract. In seven subjects blood samples were drawn every 15 minutes for radioimmunoassay of motilin and somatostatin. After two phase 3s of the migrating motor complex, 6 mg of sumatriptan was administered subcutaneously. Recording continued until two more phase 3s had occurred.Results—Sumatriptan induced a premature phase 3 in the jejunum after a median of 10 (8) minutes. The duration of the migrating motor complex cycle was shortened at the expense of phase 2. After sumatriptan, plasma somatostatin concentrations were reduced and gastric phase 3s were suppressed, although median motilin concentrations and the occurrence of plasma motilin peaks were not affected. Phase 3s of the migrating motor complex preceding sumatriptan were associated with motilin peaks, while phase 3s after sumatriptan were not. Furthermore, pretreatment with sumatriptan prevented the induction of a gastric phase 3 by the motilin agonist erythromycin.Conclusions—Administration of the 5HT1P receptor agonist sumatriptan induces a premature intestinal phase 3, suppresses gastric phase 3s, prevents induct- ion of a gastric phase 3 by erythromycin, and reduces plasma somatostatin concentrations.


1996 ◽  
Vol 41 (3) ◽  
pp. 522-527 ◽  
Author(s):  
Leonardo Marzio ◽  
Laurino Grossi ◽  
Mariassunta Falcucci ◽  
Antonio Francesco Ciccaglione ◽  
Maria Grazia Malatesta ◽  
...  

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