The role of acetylcholine in the regulation of ion transport by rat colon mucosa

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Abstract
Acetylcholine increased the potential difference across rat proximal colon in vivo and in vitro. There was a sigmoid relationship between change in potential difference and logarithm of the acetylcholine dose. The dose-response curve was shifted to the left by neostigmine and to the right by atropine, suggesting that acetylcholine action was mediated by a muscarinic type of receptor. The dose-response curve for acetylcholine in vivo was not altered by ganglion-blocking agents hexamethonium and pentolinium, suggesting a direct effect of this transmitter on the colon. Acetylcholine caused an increase in potential difference, a small decrease in resistance and hence a rise in the current generated by normal and stripped everted sacs of rat colon. In the absence of Na+, the calculated current change produced by acetylcholine was reduced, and removal of Cl- had a similar inhibitory effect. The absence of bicarbonate did not significantly affect the response. Acetylcholine virtually abolished net Na+ movement and induced net Cl- secretion, and these changes accounted for the increased short-circuit current. Acetylcholine had no effect on O2 consumption by rings of colon. Tracts staining for acetylcholinesterase were observed running from the submucous plexus towards the mucosal epithelium. Acetylcholine apparently can influence ion movement by rat colonic mucosa and the autonomic nervous system might be involved in regulation of transport mechanisms in this tissue.