Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
2010-12-14
pubmed:abstractText
This study investigated the expression of A(1) and A(2A) receptors in the rat colonic neuromuscular compartment, and characterized their roles in the control of motility during inflammation. Colitis was induced by 2,4-dinitrobenzenesulfonic acid. A(1), A(2A) receptors, and ecto-5'-nucleotidase (CD73, adenosine producing enzyme) mRNA expression was examined by RT-PCR. The effects of DPCPX (A(1) receptor antagonist), CCPA (A(1) receptor agonist), 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol (A(2A) receptor antagonist), 4-[2-[[6-amino-9-(N-ethyl-b-D-ribofuranuronamidosyl)-9H-purin-2-yl]amino]ethyl]benzenepropanoic acid hydrochloride (A(2A) receptor agonist), AOPCP (CD73 inhibitor) were tested on electrically or carbachol-evoked contractions in colonic longitudinal muscle preparations. In normal colon, RT-PCR revealed the presence of A(1) receptors, A(2A) receptors and CD73, and an increased expression of A(2A) receptors and CD73 was detected in inflamed tissues. In normal colon, DPCPX or 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol enhanced electrically-induced contractions, while in inflamed preparations the effect of DPCPX no longer occurred. In normal colon, CCPA or 4-[2-[[6-amino-9-(N-ethyl-b-D-ribofuranuronamidosyl)-9H-purin-2-yl]amino]ethyl] benzenepropanoic acid hydrochloride decreased electrically-induced contractions. Under inflammation, 4-[2-[[6-amino-9-(N-ethyl-b-D-ribofuranuronamidosyl)-9H-purin-2-yl]amino]ethyl] benzenepropanoic acid hydrochloride reduced electrically evoked contractions with higher efficacy, while the inhibition by CCPA remained unchanged. A(1) and A(2A) receptor ligands did not affect carbachol-induced contractions. AOPCP enhanced electrically-induced contractions and prevented the contractile effects of 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol, without interfering with DPCPX, both in normal and inflamed colons. These results indicate that, in normal colon, both A(1) and A(2A) receptors contribute to the inhibitory control of motor functions at neuronal level. Under bowel inflammation, A(1) receptor loses its modulating actions, while the recruitment of A(2A) receptor by CD73-dependent endogenous adenosine drives an enhanced inhibitory control of colonic neuromotility.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/1,3-dipropyl-8-cyclopentylxanthine, http://linkedlifedata.com/resource/pubmed/chemical/2,4-dinitrobenzenesulfonic acid, http://linkedlifedata.com/resource/pubmed/chemical/2-chloro-N(6)cyclopentyladenosine, http://linkedlifedata.com/resource/pubmed/chemical/5'-Nucleotidase, http://linkedlifedata.com/resource/pubmed/chemical/Adenosine, http://linkedlifedata.com/resource/pubmed/chemical/Adenosine A1 Receptor Agonists, http://linkedlifedata.com/resource/pubmed/chemical/Adenosine A1 Receptor Antagonists, http://linkedlifedata.com/resource/pubmed/chemical/Adenosine A2 Receptor Agonists, http://linkedlifedata.com/resource/pubmed/chemical/Adenosine A2 Receptor Antagonists, http://linkedlifedata.com/resource/pubmed/chemical/Benzenesulfonates, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Adenosine A1, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adenosine A2, http://linkedlifedata.com/resource/pubmed/chemical/Xanthines
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1879-0712
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
650
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
639-49
pubmed:meshHeading
pubmed-meshheading:21034735-5'-Nucleotidase, pubmed-meshheading:21034735-Adenosine, pubmed-meshheading:21034735-Adenosine A1 Receptor Agonists, pubmed-meshheading:21034735-Adenosine A1 Receptor Antagonists, pubmed-meshheading:21034735-Adenosine A2 Receptor Agonists, pubmed-meshheading:21034735-Adenosine A2 Receptor Antagonists, pubmed-meshheading:21034735-Animals, pubmed-meshheading:21034735-Benzenesulfonates, pubmed-meshheading:21034735-Colitis, pubmed-meshheading:21034735-Colon, pubmed-meshheading:21034735-Disease Models, Animal, pubmed-meshheading:21034735-Male, pubmed-meshheading:21034735-Muscle, Smooth, pubmed-meshheading:21034735-Muscle Contraction, pubmed-meshheading:21034735-Rats, pubmed-meshheading:21034735-Rats, Sprague-Dawley, pubmed-meshheading:21034735-Receptor, Adenosine A1, pubmed-meshheading:21034735-Receptors, Adenosine A2, pubmed-meshheading:21034735-Xanthines
pubmed:year
2011
pubmed:articleTitle
Differential recruitment of high affinity A1 and A2A adenosine receptors in the control of colonic neuromuscular function in experimental colitis.
pubmed:affiliation
Division of Pharmacology and Chemotherapy, Department of Internal Medicine, University of Pisa, Pisa, Italy.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't