Open AccessMicroalbuminuria versus brain natriuretic peptide in cardiac hypertrophy of hypertensive rats
Author(s) -
Youakim Saliba,
Éliane Chouery,
André Megarbané,
Henry N. Jabbour,
Nassim Farès
Publication year - 2010
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.931826
Subject(s) - microalbuminuria , medicine , brain natriuretic peptide , endocrinology , left ventricular hypertrophy , muscle hypertrophy , blood pressure , creatinine , captopril , natriuretic peptide , cardiology , heart failure
The objective of this study was to assess a possible link betweenmicroalbuminuria (MA), a major risk factor of the cardiorenalsyndrome and the brain natriuretic peptide (BNP), a marker ofcardiac hypertrophy. Two kidney-one clip (2K-1C) renovascularhypertension was induced in 24 male Wistar rats (weighing 220-250 g). Rats were randomized into four groups for 8 weeks:Sham, not treated; Bos, treated with bosentan; Cap, treated withcaptopril; Bos/Cap, treated with both drugs. Blood pressure,plasma BNP and transforming growth factor β1 (TGF-β1)concentrations, microalbuminuria and creatininemia as well ascardiac mass, BNP, α- and β-myosin heavy chain (MHC) geneexpression and kidney histology were determined. Followingstenosis, Sham rats developed hypertension (p<0.001), anincrease in BNP (p<0.05) and TGF-β1 (p<0.005) concentrations,creatinine levels (p<0.001), and urinary albumin (p<0.001).Under drug treatment, decreases in blood pressure (p<0.001),creatinine levels (p<0.05), plasma TGF-β1 (p<0.005) and BNP(p<0.05) concentrations, were concomitant with the absence ofMA which was significantly correlated with reductions in cardiacmass (p<0.05) and hypertrophy markers (BNP and β-MHC geneexpression) (p<0.005) as well as in renal fibrosis. These findingssuggest a potential link between microalbuminuria evolution andBNP as well as a possible effect of microalbuminuria-loweringtherapy on halting the progression, or even inducing theregression of cardiac hypertrophy.