Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-12-17
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Anesthetics, Local, http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents..., http://linkedlifedata.com/resource/pubmed/chemical/Antipsychotic Agents, http://linkedlifedata.com/resource/pubmed/chemical/Benzamides, http://linkedlifedata.com/resource/pubmed/chemical/Indomethacin, http://linkedlifedata.com/resource/pubmed/chemical/Neurokinin A, http://linkedlifedata.com/resource/pubmed/chemical/Neurotransmitter Agents, http://linkedlifedata.com/resource/pubmed/chemical/Piperidines, http://linkedlifedata.com/resource/pubmed/chemical/Quinuclidines, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Neurokinin-1, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Neurokinin-2, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Neurokinin-3, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tachykinin, http://linkedlifedata.com/resource/pubmed/chemical/SR 140333, http://linkedlifedata.com/resource/pubmed/chemical/SR 142801, http://linkedlifedata.com/resource/pubmed/chemical/SR 48968, http://linkedlifedata.com/resource/pubmed/chemical/Substance P, http://linkedlifedata.com/resource/pubmed/chemical/Tetrodotoxin, http://linkedlifedata.com/resource/pubmed/chemical/Trinitrobenzenesulfonic Acid
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0163-2116
pubmed:author
pubmed:issnType
Print
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
220-8
pubmed:meshHeading
pubmed-meshheading:17510797-Anesthetics, Local, pubmed-meshheading:17510797-Animals, pubmed-meshheading:17510797-Anti-Inflammatory Agents, Non-Steroidal, pubmed-meshheading:17510797-Antipsychotic Agents, pubmed-meshheading:17510797-Benzamides, pubmed-meshheading:17510797-Colitis, pubmed-meshheading:17510797-Disease Models, Animal, pubmed-meshheading:17510797-Indomethacin, pubmed-meshheading:17510797-Intestinal Mucosa, pubmed-meshheading:17510797-Male, pubmed-meshheading:17510797-Neurokinin A, pubmed-meshheading:17510797-Neurotransmitter Agents, pubmed-meshheading:17510797-Piperidines, pubmed-meshheading:17510797-Quinuclidines, pubmed-meshheading:17510797-Rats, pubmed-meshheading:17510797-Rats, Sprague-Dawley, pubmed-meshheading:17510797-Receptors, Neurokinin-1, pubmed-meshheading:17510797-Receptors, Neurokinin-2, pubmed-meshheading:17510797-Receptors, Neurokinin-3, pubmed-meshheading:17510797-Receptors, Tachykinin, pubmed-meshheading:17510797-Stereoisomerism, pubmed-meshheading:17510797-Substance P, pubmed-meshheading:17510797-Tetrodotoxin, pubmed-meshheading:17510797-Trinitrobenzenesulfonic Acid
pubmed:year
2008
pubmed:articleTitle
Chronic inflammation alters the contribution of neurokinin receptor subtypes to epithelial function in rat colon.
pubmed:affiliation
Department of Physiology & Pharmacology, Ponce School of Medicine, Ponce, PR 00732-7004, USA. cappleyard@psm.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural