Microalbuminuria versus brain natriuretic peptide in cardiac hypertrophy of hypertensive rats

Title:

Microalbuminuria versus brain natriuretic peptide in cardiac hypertrophy of hypertensive rats

Creator:

Saliba, Y., Chouery, E., Mégarbané, A., Jabbour, H., and Farès, N.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:fe9804f1-c3d9-4203-866b-983f221b09c7
uuid:fe9804f1-c3d9-4203-866b-983f221b09c7
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, hypertenze, hypertension, microalbuminuria, brain natriuretic peptide, cardiac hypertrophy, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

The objective of this study was to assess a possible link between microalbuminuria (MA), a major ri sk factor of the cardiorenal syndrome 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 220-250 g). Rats were randomized into four 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, microalbuminuria and creatininemia as well as cardiac mass, BNP, α- and β-myosin heavy chain (MHC) gene expression and kidney histology were determined. Following stenosis, Sham rats developed hypertension (p<0.001), an increase 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 co ncomitant 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 microalbuminuria evolution and BNP as well as a possible effect of microalbuminuria-lowering therapy on halting the progression, or even inducing the regression of cardiac hypertrophy., Y. Saliba, E. Chouery, A. Mégarbané, H. Jabbour, N. Farès., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2010 Volume:59 | Number:6

Harvested from:

CDK

Metadata only:

false