Many studies documented the relationship between elevated plasma concentrations of natriuretic peptides and cardiovascular diseases, especially heart failure. However, it is still uncertain whether physical exercise leads to a significant release of natriuretic peptide in healthy subjects. The aim of this study was to determine the effect of maximal physical activity on plasma BNP concentrations in healthy individuals within 3 hours after the short-term exercise. BNP plasma concentrations were measured in 15 healthy volunteers before, immediately after as well as 1 hour and 3 hours after bicycle spiroergometry. Maximal workload and exercise capacity were assessed in watts, wattseconds, metabolic equivalents and VO2max. Mean BNP plasma levels before, immediately after, 1 hour and 3 hours postexercise were 19.4±2.5; 30.6±4.7; 17.9±2.5 and 18.7±3.1 pg/ml, respectively. The increase of BNP concentrations immediately after exercise was statistically significant (p=0.0017) compared to baseline values. We did not find any correlation between the post-exercise increase of BNP levels and age, body mass index, maximal workload or exercise capacity. In conclusion, short-term maximal physical exercise in healthy individuals led to a fast and transient rise of plasma BNP concentrations, which remained well within normal range and far below the cut-off value for heart failure (100 pg/ml)., J. Krupička ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
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