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Carbachol-stimulated chloride secretion in mouse colon: evidence of a role for autocrine prostaglandin E2 release

Published online by Cambridge University Press:  25 January 2001

Mark A. Carew  and
Peter Thorn
Mark A. Carew
Affiliation:
Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QJ, UK
Peter Thorn
Affiliation:
Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QJ, UK
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Abstract

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 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 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.

Type
Research Article
Information
Experimental Physiology , Volume 85 , Issue 1 , January 2000 , pp. 67 - 72
Copyright
© The Physiological Society 2000

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