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Carbachol‐Stimulated Chloride Secretion in Mouse Colon: Evidence of a Role for Autocrine Prostaglandin E 2 Release
Author(s) -
Carew Mark A.,
Thorn Peter
Publication year - 2000
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1111/j.1469-445x.2000.01947.x
Subject(s) - carbachol , secretion , autocrine signalling , endocrinology , medicine , prostaglandin e2 , chemistry , prostaglandin , prostaglandin e , crypt , biology , stimulation , receptor
We used the short‐circuit current technique to investigate the possible facilitatory role of epithelium‐derived prostaglandin E 2 (PGE 2 ) release on Cl − secretion in the mouse colon. Carbachol‐ (CCh)‐stimulated Cl − secretion was reduced by pretreatment with either indomethacin (10 μM), or TTX (1 μM), 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 PGE 2 (1 nM). In acutely isolated, unstimulated crypt cells, we measured PGE 2 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.