The effect of a continuous infusion of human brain natriuretic peptide, 2 p
mol.min(-1).kg(-1), during 60 min was studied in nine patients with congest
ive heart failure and in 10 healthy control subjects. Brain natriuretic pep
tide increased from 1.6 to 101 pmol/l in control subjects and from 25 to 17
3 pmol/l in congestive heart failure during infusion. Urinary sodium excret
ion increased significantly in both congestive heart failure (60%) and cont
rol subjects (71%), but the absolute increase was significantly lower in co
ngestive heart failure (27 mu mol/min) than in control subjects (190 mu mol
/min). Urinary flow rate did nor change. The lithium clearance technique wa
s used to evaluate the segmental tubular function; the distal fractional re
absorption of sodium decreased significantly less in congestive heart failu
re (DFRNa: -0.8%) than in control subjects (DFRNa: -3.7%). Baseline values
for glomerular filtration rate and renal plasma flow were reduced in conges
tive heart failure, but brain natriuretic peptide induced no significant ch
anges between congestive heart failure and control subjects. Brain natriure
tic peptide induced the same absolute increase in secondary messenger cGMP
in plasma and urine in both patients and healthy subjects, it is concluded
that the natriuretic response to brain natriuretic peptide infusion was imp
aired in patients with congestive heart failure compared with healthy subje
cts, and it is likely that the im paired natriuretic response was caused by
a reduced responsiveness in the distal part of the nephron.