Evidence for an opiate-mediated pyloric sphincter reflex.

Abstract

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.