Send to

Choose Destination
See comment in PubMed Commons below
Dig Dis Sci. 2008 Jan;53(1):220-8. Epub 2007 May 18.

Chronic inflammation alters the contribution of neurokinin receptor subtypes to epithelial function in rat colon.

Author information

Department of Physiology & Pharmacology, Ponce School of Medicine, Ponce, PR 00732-7004, USA.


We have previously shown that neurokinin-1 (NK1) receptors predominantly mediate substance P-induced secretion of the non-inflamed rat colonic mucosa in vitro with a gradient in the magnitude of these responses. The aim of this study was to examine the effects of chronic inflammation on the contributions of different neurokinin receptor subtypes to colonic mucosal secretion. Colitis was induced by the intracolonic administration of 2,4,6-trinitrobenzene sulfonic acid in rats, reactivated 6 weeks later. Segments of proximal, mid- and distal colon were stripped of muscularis propria and mounted in Ussing chambers for measurement of short-circuit current. Use of selective agonists suggests that in the chronically inflamed rat colon NK1 receptors play a greater role in neurokinin-mediated mucosal secretion than do either NK2 or NK3. Selective antagonism implies that this is region-specific, with the inflammatory process altering the relative contribution of the neurokinin receptor subtypes within each region of the rat colon.

[Indexed for MEDLINE]

Publication type, MeSH terms, Substances, Grant support

Publication type

MeSH terms


Grant support

PubMed Commons home

PubMed Commons


    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center