MA vs BNP in Cardiac Hypertrophy Microalbuminuria versus Brain Natriuretic Peptide in Cardiac Hypertrophy of Hypertensive Rats

The objective of this study is to assess a possible link between microalbuminuria (MA), a major risk factor of the cardiorenal syndrome (CRS) and the brain natriuretic peptide (BNP), a marker of cardiac hypertrophy. Two kidney-one clip (2K-1C) renovascular hypertension was induced in 24 male Wistar rats weighing (220-250g). Rats were then randomized into 4 groups for 8 weeks: Sham, not treated; Bos, treated with bosentan; Cap, treated with captopril; Bos/Cap, treated with both drugs. Blood pressure, plasma BNP and transforming growth factor β1 (TGF-β1) concentrations, MA and creatininaemia were ascertained, as well as cardiac mass, BNP, αand βmyosin heavy chain (MHC) gene expression and kidney histology. Following stenosis, Sham rats developed hypertension (p<0.001), an increase in BNP (p<0.05) and TGF-β1 (p<0.005) concentrations, creatininaemia (p<0.001), and urinary albumin (p<0.001). Decreases under treatment, in blood pressure (p<0.001), creatininaemia (p<0.05), plasma TGF-β1 (p<0.005) and BNP (p<0.05) concentrations, were concomitant with the absence of MA which was significantly correlated with reductions in cardiac mass (p<0.05) and hypertrophy markers (BNP and β-MHC gene expression) (p<0.005) as well as in renal fibrosis. These findings, suggest a potential link between MA evolution and BNP, as well as a possible effect of MAlowering therapy on halting the progression, or even inducing the regression of cardiac hypertrophy.