Brain natriuretic peptide (BNP) effects were abolished in rats with congestive heart failure compared to controls, despite plasma BNP levels being more than four-fold higher.
Does brain natriuretic peptide (BNP) have altered hemodynamic and renal effects in rats with experimental congestive heart failure compared to control rats?
In a rat model of CHF, there is resistance to the hypotensive, diuretic, and natriuretic effects of BNP despite elevated plasma levels, contributing to sodium retention.
The hemodynamic and renal effects of brain natriuretic peptide (BNP) were studied in conscious rats with experimental congestive heart failure (CHF) produced by an aortocaval fistula. The peptide had potent hypotensive, diuretic, and natriuretic effects in control rats, all of which were abolished in CHF. Plasma levels of BNP increased time-dependently during the development of CHF, and were more than four-fold higher in sodium retaining rats than in control rats. The data suggest that BNP secretion from the atria is increased in CHF, and that resistance to BNP, in addition to the relative resistance to atrial natriuretic factor, may contribute to sodium retention in CHF.
Hoffman et al. (1991) studied Congestive heart failure (CHF). Brain natriuretic peptide (BNP) vs. Control rats was evaluated on Hemodynamic and renal effects and plasma BNP levels. Brain natriuretic peptide (BNP) effects were abolished in rats with congestive heart failure compared to controls, despite plasma BNP levels being more than four-fold higher.