AJP - Gastrointestinal and Liver Physiology, Vol 246, Issue 2 130-G136, Copyright © 1984 by American Physiological Society
Evidence for an opiate-mediated pyloric sphincter reflex
J. C. Reynolds, A. Ouyang and S. Cohen
The purpose of this study was to determine the mechanism by which the
feline pylorus contracts in response to duodenal acidification.
Simultaneous intraluminal pressures and serosal electrical activity were
recorded from the antrum, pylorus, and duodenum of the anesthetized cat.
The pylorus demonstrated a narrow zone of tonically increased pressure.
Duodenal but not antral acidification increased the frequency and amplitude
of phasic spike-associated pyloric contractions (P less than 0.001). This
response was antagonized by tetrodotoxin, intraluminal (ethyl
aminobenzoate), or naloxone. Bilateral cervical vagotomy, atropine,
phentolamine, propranolol, cinanserine, diphenhydramine, or cimetidine had
no effect on the pyloric response to duodenal acidification. Duodenal spike
activity was also increased by duodenal acidification but was antagonized
by atropine and not by naloxone. Leucine- or methionine-enkephalin
intra-arterially produced dose-dependent increases in phasic pyloric
contractions. The EDmax for leucin-enkephalin was 1.0 microgram/kg. The
enkephalins inhibited duodenal spike activity in a dose-dependent fashion.
These studies suggest that the pyloric spike-associated, high-amplitude
phasic contractions in response to duodenal acidification involve local
neural pathways that may be mediated through an opioid peptide. The pyloric
response to duodenal acidification is distinguished from that of the
duodenum, which is cholinergic.
