omega-conotoxin-(conus-magus) and propionic-acid

Short chain fatty acids stimulate Cl secretion in rat descending colon in vitro via an enteric reflex involving mucosa and cholinergic nerves. We used the short circuit current as the measure of Cl secretion caused by Na propionate (NaP) (0.5 mM) in luminal bath fluid and studied the mechanism of the response. The NaP response was decreased 81% by atropine and 76% by lidocaine. It was unaffected by tetrodotoxin, omega-conotoxin or by tachyphylaxis to capsaicin, CGRP, substance P, histamine or PGE2. It was not reduced by inhibitors of 5-HT2 or 5HT3 receptors or by partial tachyphylaxis to 5-HT. However, superficial mucosal injury with hypertonic Na sulfate (2 M) or xylose (4.5 M) reduced the NaP response by 90% and 86%, respectively, and mucosal concanavalin A (1 mg/ml) reduced it by 73%. Neither piroxicam (10 microM) nor nordihydroguaretic acid (10 microM) affected the NaP response. We hypothesize that NaP stimulates the superficial epithelium to release an unidentified agonist that depolarizes predominantly cholinergic nerve terminals and causes colonic secretion.

Topics: Acetylcholine; Animals; Atropine; Calcium Channel Blockers; Chlorides; Colon; Dinoprostone; Electric Stimulation; Female; Guinea Pigs; Hexamethonium Compounds; Histamine; Humans; In Vitro Techniques; Lidocaine; Male; Nerve Endings; Neuropeptides; omega-Conotoxins; Peptides; Piroxicam; Propionates; Rabbits; Rats; Serotonin; Serotonin Antagonists; Tachyphylaxis; Tetrodotoxin