Brain natriuretic peptide (BNP) is predominantly a cardiac ventricular horm
one that promotes natriuresis and diuresis, inhibits the renin-anglotensin-
aldosterone axis, and is a vasodilator. Plasma BNP levels are raised in ess
ential hypertension, and more so in left ventricular (LV) hypertrophy and h
eart failure. Plasma BNP levels are also elevated in ischemic heart disease
. Attempts have been made to use plasma BNP levels as a marker of LV dysfun
ction, but these have shown that plasma BNP levels are probably not sensiti
ve enough to replace echocardiography in the diagnosis of LV dysfunction. P
ericardial BNP or N-BNP may be more suitable markers of LV dysfunction. Pla
sma BNP levels are also elevated in right ventricular dysfunction, pregnanc
y-induced hypertension, aortic stenosis, age, subarachnoid hemorrhage, card
iac allograft rejection and cavopulmonary connection, and BNP may have an i
mportant pathophysiological role in some or all of these conditions. Clinic
al trials have demonstrated the natriuretic, diuretic and vasodilator effec
ts, as well as inhibitory effects on renin and aldosterone of infused synth
etic human BNP (nesiritide) in healthy humans. BNP infusion improves LV fun
ction in patients with congestive heart failure via a vasodilating and a pr
ominent natriuretic effect. BNP infusion is useful for the treatment of dec
ompensated congestive heart failure requiring hospitalization. The clinical
potential of BNP is limited as it is a peptide and requires infusion. Drug
s that modify the effects of BNP are furthering our understanding of the pa
thophysiological role and clinical potential of BNP. Increasing the effects
of BNP may be a useful therapeutic approach in heart failure involving LV
dysfunction. The levels of plasma BNP are increased by blockers, cardiac gl
ycosides and vasopeptidase inhibitors, and this may contribute to the usefu
lness of these agents in heart failure. (C) 2001 Prous Science. All rights
reserved.