Linked Life Data

16188279

Source:http://linkedlifedata.com/resource/pubmed/id/16188279

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2006-1-23
pubmed:abstractText
Proteinase-activated receptor (PAR)-1 or -2 modulates gastrointestinal transit in vivo. To clarify the underlying mechanisms, we characterized contraction/relaxation caused by TFLLR-NH2 and SLIGRL-NH2, PAR-1- and -2-activating peptides, respectively, in gastric and small intestinal (duodenal, jejunal and ileal) smooth muscle isolated from wild-type and PAR-2-knockout mice. Either SLIGRL-NH2 or TFLLR-NH2 caused both relaxation and contraction in the gastrointestinal preparations from wild-type animals. Apamin, a K+ channel inhibitor, tended to enhance the peptide-evoked contraction in some of the gastrointestinal preparations, whereas it inhibited relaxation responses to either peptide completely in the stomach, but only partially in the small intestine. Indomethacin reduced the contraction caused by SLIGRL-NH2 or TFLLR-NH2 in both gastric and ileal preparations, but unaffected apamin-insensitive relaxant effect of either peptide in ileal preparations. Repeated treatment with capsaicin suppressed the contractile effect of either peptide in the stomach, but not clearly in the ileum, whereas it enhanced the apamin-insensitive relaxant effect in ileal preparations. In any gastrointestinal preparations from PAR-2-knockout mice, SLIGRL-NH2 produced no responses. Thus, the inhibitory component in tension modulation by PAR-1 and -2 involves both apamin-sensitive and -insensitive mechanisms in the small intestine, but is predominantly attributable to the former mechanism in the stomach. The excitatory component in the PAR-1 and -2 modulation may be mediated, in part, by activation of capsaicin-sensitive sensory nerves and/or endogenous prostaglandin formation. Our study thus clarifies the multiple mechanisms for gastrointestinal motility modulation by PAR-1 and -2, and also provides ultimate evidence for involvement of PAR-2.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
78
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
950-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16188279-Animals, pubmed-meshheading:16188279-Anti-Inflammatory Agents, Non-Steroidal, pubmed-meshheading:16188279-Apamin, pubmed-meshheading:16188279-Calcium Channel Blockers, pubmed-meshheading:16188279-Capsaicin, pubmed-meshheading:16188279-Female, pubmed-meshheading:16188279-Gastrointestinal Motility, pubmed-meshheading:16188279-Indomethacin, pubmed-meshheading:16188279-Intestines, pubmed-meshheading:16188279-Isometric Contraction, pubmed-meshheading:16188279-Mice, pubmed-meshheading:16188279-Mice, Inbred C57BL, pubmed-meshheading:16188279-Mice, Knockout, pubmed-meshheading:16188279-Muscle Relaxation, pubmed-meshheading:16188279-Neurons, Afferent, pubmed-meshheading:16188279-Oligopeptides, pubmed-meshheading:16188279-Potassium Channels, pubmed-meshheading:16188279-Prostaglandins, pubmed-meshheading:16188279-Receptor, PAR-1, pubmed-meshheading:16188279-Receptor, PAR-2, pubmed-meshheading:16188279-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16188279-Stomach
pubmed:year
2006
pubmed:articleTitle
Mechanisms for modulation of mouse gastrointestinal motility by proteinase-activated receptor (PAR)-1 and -2 in vitro.
pubmed:affiliation
Division of Physiology and Pathophysiology, School of Pharmaceutical Sciences, Kinki University, 3-4-1 Kowakae, Higashi-Osaka, Osaka 577-8502, Japan.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't