Carbachol-stimulated chloride secretion in mouse colon: evidence of a role for autocrine prostaglandin E2 release.
We used the short-circuit current technique to investigate the possible facilitatory role of epithelium-derived prostaglandin E2 (PGE2) release on Cl- secretion in the mouse colon. Carbachol- (CCh)-stimulated Cl- secretion was reduced by pretreatment with either indomethacin (10 microM), or TTX (1 microM), and when added together, these inhibitors revealed net CCh-stimulated K+ secretion. CCh-stimulated Cl- secretion was partially restored to TTX/indomethacin-treated colons by addition of a subsecretory concentration of PGE2 (1 nM). In acutely isolated, unstimulated crypt cells, we measured PGE2 release at a similar level. We conclude that autocrine release of PGs from epithelial cells is sufficient to support the CCh-induced Cl- secretory response and is a likely co-factor in this response.
Carew
M A
MA
Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QJ, UK. carew@niehs.nih.gov
Thorn
P
P
D000818:Animals; D019898:Autocrine Communication / Q000187:drug effects*; D002217:Carbachol / Q000494:pharmacology*; D002712:Chlorides / Q000378:metabolism*; D003106:Colon / Q000187:drug effects / Q000378:metabolism*; D015232:Dinoprostone / Q000378:metabolism*; D004594:Electrophysiology; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D004848:Epithelium / Q000187:drug effects / Q000378:metabolism; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D051379:Mice; D018721:Muscarinic Agonists / Q000494:pharmacology*; D011451:Prostaglandin-Endoperoxide Synthases / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology
D002712:Chlorides; D018721:Muscarinic Agonists; D013779:Tetrodotoxin; D002217:Carbachol; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone; D007213:Indomethacin