RGD Reference Report - Chronic renal failure alters endothelial function in cerebral circulation in mice. - Rat Genome Database

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Chronic renal failure alters endothelial function in cerebral circulation in mice.

Authors: Bugnicourt, JM  Da Silveira, C  Bengrine, A  Godefroy, O  Baumbach, G  Sevestre, H  Bode-Boeger, SM  Kielstein, JT  Massy, ZA  Chillon, JM 
Citation: Bugnicourt JM, etal., Am J Physiol Heart Circ Physiol. 2011 Sep;301(3):H1143-52. Epub 2011 Jun 24.
RGD ID: 6903287
Pubmed: PMID:21705678   (View Abstract at PubMed)
DOI: DOI:10.1152/ajpheart.01237.2010   (Journal Full-text)

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-gamma (PPARgamma)]; 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 PPARgamma (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.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
end stage renal disease  ISOApoe (Mus musculus)6903287; 6903287 RGD 
end stage renal disease  IMP 6903287 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Apoe  (apolipoprotein E)

Genes (Mus musculus)
Apoe  (apolipoprotein E)

Genes (Homo sapiens)
APOE  (apolipoprotein E)


Additional Information