Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2011-8-31
pubmed:abstractText
We examined structure, composition, and endothelial function in cerebral arterioles after 4 wk of chronic renal failure (CRF) in a well-defined murine model (C57BL/6J and apolipoprotein E knockout female mice). We also determined quantitative expression of endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (on serine 1177 and threonine 495), and caveolin-1; quantitative expression of markers of vascular inflammation or oxidative stress [Rock-1, Rock-2, VCAM-1, and peroxisome proliferator-activated receptor-? (PPAR?)]; and the plasma concentration of L-arginine and asymmetric dimethylarginine (ADMA). Our hypothesis was that endothelial function would be impaired in cerebral arterioles during CRF following either a decrease in NO production (through alteration of eNOS expression or regulation) or an increase in NO degradation (due to oxidative stress or vascular inflammation). Endothelium-dependent relaxation was impaired during CRF, but endothelium-independent relaxation was not. CRF had no effect on cerebral arteriolar structure and composition. Quantitative expressions of eNOS, eNOS phosphorylated on serine 1177, caveolin-1, Rock-1, Rock-2, and VCAM-1 were similar in CRF and non-CRF mice. In contrast, quantitative expression of PPAR? (which exercises a protective role on blood vessels) was significantly lower in CRF mice, whereas quantitative expression of eNOS phosphorylated on the threonine 495 (the inactive form of eNOS) was significantly higher. Lastly, the plasma concentration of ADMA (a uremic toxin and an endogenous inhibitor of eNOS) was elevated and plasma concentration of L-arginine was low in CRF. In conclusion, endothelial function is impaired in a mouse model of early stage CRF. These alterations may be related (at least in part) to a decrease in NO production.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins E, http://linkedlifedata.com/resource/pubmed/chemical/Arginine, http://linkedlifedata.com/resource/pubmed/chemical/Cav1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Caveolin 1, http://linkedlifedata.com/resource/pubmed/chemical/Inflammation Mediators, http://linkedlifedata.com/resource/pubmed/chemical/N,N-dimethylarginine, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type III, http://linkedlifedata.com/resource/pubmed/chemical/Nos3 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/PPAR gamma, http://linkedlifedata.com/resource/pubmed/chemical/Rock1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Rock2 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Vascular Cell Adhesion Molecule-1, http://linkedlifedata.com/resource/pubmed/chemical/Vasodilator Agents, http://linkedlifedata.com/resource/pubmed/chemical/rho-Associated Kinases
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1522-1539
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
301
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1143-52
pubmed:meshHeading
pubmed-meshheading:21705678-Analysis of Variance, pubmed-meshheading:21705678-Animals, pubmed-meshheading:21705678-Apolipoproteins E, pubmed-meshheading:21705678-Arginine, pubmed-meshheading:21705678-Arterioles, pubmed-meshheading:21705678-Blotting, Western, pubmed-meshheading:21705678-Caveolin 1, pubmed-meshheading:21705678-Cerebrovascular Circulation, pubmed-meshheading:21705678-Cerebrovascular Disorders, pubmed-meshheading:21705678-Disease Models, Animal, pubmed-meshheading:21705678-Dose-Response Relationship, Drug, pubmed-meshheading:21705678-Endothelium, Vascular, pubmed-meshheading:21705678-Female, pubmed-meshheading:21705678-Inflammation Mediators, pubmed-meshheading:21705678-Kidney Failure, Chronic, pubmed-meshheading:21705678-Mice, pubmed-meshheading:21705678-Mice, Inbred C57BL, pubmed-meshheading:21705678-Mice, Knockout, pubmed-meshheading:21705678-Nephrectomy, pubmed-meshheading:21705678-Nitric Oxide, pubmed-meshheading:21705678-Nitric Oxide Synthase Type III, pubmed-meshheading:21705678-PPAR gamma, pubmed-meshheading:21705678-Phosphorylation, pubmed-meshheading:21705678-Pia Mater, pubmed-meshheading:21705678-Vascular Cell Adhesion Molecule-1, pubmed-meshheading:21705678-Vasodilation, pubmed-meshheading:21705678-Vasodilator Agents, pubmed-meshheading:21705678-rho-Associated Kinases
pubmed:year
2011
pubmed:articleTitle
Chronic renal failure alters endothelial function in cerebral circulation in mice.
pubmed:affiliation
Institut National de Santé et de Recherche Médicale, ERI12, Amiens, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't