Behar J, Biancani P
Gastroenterology. 1984 Jan;86(1):134-41.
The effect and physiologic role of enkephalins on the sphincter of Oddi was studied in the cat. Leucine- and methionine-enkephalin caused an initial sphincter of Oddi contraction followed by a more prolonged relaxation. The excitatory effect of leucine-enkephalin was antagonized partially by atropine and by methysergide infusion. It was completely blocked by a combination of atropine and methysergide infusion, by tetrodotoxin, by 5-hydroxytryptamine depletion induced by reserpine, and by 5-hydroxytryptamine tachyphylaxis. Naloxone infusion decreased sphincter of Oddi motor activity, which was reversed by tetrodotoxin. Maximal sphincter of Oddi relaxation was induced by doses of naloxone (40 micrograms/kg) that antagonized a maximal dose of morphine. Higher doses of naloxone (640 micrograms/kg) were needed to block maximal doses of enkephalin (8 micrograms/kg). The enkephalin inhibitory action was blocked only by tetrodotoxin. These findings indicate that (a) leucine-enkephalin has two receptor sites on the sphincter of Oddi--one at the serotonergic neurons and the other at noncholinergic, nonadrenergic inhibitory neurons, and (b) opioid peptides participate in the intramural excitatory pathway to the sphincter of Oddi.