RGD Reference Report - Cardiorenal syndrome in hypertensive rats: microalbuminuria, inflammation and ventricular hypertrophy. - Rat Genome Database

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Cardiorenal syndrome in hypertensive rats: microalbuminuria, inflammation and ventricular hypertrophy.

Authors: Moubarak, M  Jabbour, H  Smayra, V  Chouery, E  Saliba, Y  Jebara, V  Fares, N 
Citation: Moubarak M, etal., Physiol Res. 2012 Mar 6;61(1):13-24. Epub 2011 Dec 20.
RGD ID: 6907405
Pubmed: PMID:22188107   (View Abstract at PubMed)

The aim of our study was to evaluate a possible association between microalbuminuria (MA), several low-grade inflammation factors and left ventricular hypertrophy (LVH) by using a pharmacological approach. This may provide new insights into the pathophysiologic mechanisms of the cardiorenal syndrome (CRS) linking early renal impairment with elevated cardiovascular risk. Two kidney-one clip (2K-1C) renovascular hypertension was induced in 24 male Wistar rats (220-250 g). After the development of hypertension, rats were divided into four groups: 2K-1C (untreated), calcium channel blocker (amlodipine-treated), angiotensin receptor blocker (losartan-treated) and peripheral vasodilator (hydralazine-treated), which were treated for 10 weeks. Rats in the 2K-1C group had all developed hypertension, a significant increase in plasma levels of tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), brain natriuretic peptide (BNP) and C-reactive protein (CRP). Moreover MA and creatininaemia underwent a significant increase. Under treatment decreases were observed in systolic blood pressure (SBP), TNF-alpha, CRP, IL-6, BNP concentrations and creatininaemia. These results were related to the absence of MA which was significantly associated with reductions in cardiac mass and hypertrophy markers (BNP and beta-MHC gene expression) as well as renal interstitial inflammation. In conclusion, our results suggest that the reduction of MA is correlated with the decrease of the inflammatory components and seems to play an important role in protecting against cardiac hypertrophy and renal injury.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
renal hypertension  ISOCrp (Rattus norvegicus)6907405; 6907405protein:increased expression:serumRGD 
renal hypertension  IEP 6907405; 6907405; 6907405; 6907405protein:increased expression:serumRGD 
renal hypertension  ISOIl6 (Rattus norvegicus)6907405; 6907405protein:increased expression:serumRGD 
renal hypertension  ISONppb (Rattus norvegicus)6907405; 6907405protein:increased expression:serumRGD 
renal hypertension  ISOTnf (Rattus norvegicus)6907405; 6907405protein:increased expression:serumRGD 

Objects Annotated

Genes (Rattus norvegicus)
Crp  (C-reactive protein)
Il6  (interleukin 6)
Nppb  (natriuretic peptide B)
Tnf  (tumor necrosis factor)

Genes (Mus musculus)
Crp  (C-reactive protein, pentraxin-related)
Il6  (interleukin 6)
Nppb  (natriuretic peptide type B)
Tnf  (tumor necrosis factor)

Genes (Homo sapiens)
CRP  (C-reactive protein)
IL6  (interleukin 6)
NPPB  (natriuretic peptide B)
TNF  (tumor necrosis factor)


Additional Information