Effect of angiotensin-converting enzyme inhibition on plasma brain natriuretic peptide levels in patients with heart failure

Abstract

1. The aim of this study was to examine the effect of captopril, an angiotensin-converting enzyme inhibitor, on plasma levels of human brain natriuretic peptide-like immunoreactivity (hBNP-li) in patients with congestive heart failure. 2. Six male patients (aged 52–74 years) with mild to moderate congestive heart failure were studied on two occasions in the semi-recumbent position. After a 30 min rest, patients were randomized to receive oral tablets of either captopril (6.25 mg followed by 25 mg 2 h later) or placebo in a single-blind manner. Plasma hBNP-li, atrial natriuretic peptide-like immunoreactivity (ANP-li) and angiotensin II-like immunoreactivity (ANG II-li) levels and blood pressure were measured. 3. Baseline plasma hBNP-li and ANP-li levels in these patients with mild to moderate congestive heart failure were 13.5 ± 3.2 pmol/l and 50.9 ± 11.8 pmol/l, respectively. In 11 healthy male subjects aged 20–23 years, the peripheral plasma hBNP-li and ANP-li levels were 1.3 ± 0.2 pmol/l and 5.6 ± 1.7 pmol/l, respectively. In all patients, captopril decreased the plasma ANG II-li level (from 24.3 ± 8.1 to 6.6 ± 3.2 pmol/l, P<0.05) and mean arterial blood pressure (from 92 ± 3 to 80 ± 3 mmHg, P<0.05). Compared with placebo, captopril treatment was associated with significant reductions in plasma hBNP-li (from 14.3 ± 3.0 to 12.8 ± 2.1 pmol/l, P<0.05) and in plasma ANP-li (from 53.9 ± 1.11 to 36.8 ± 7.6 pmol/l, P<0.05) levels. 4. Our results show that in patients with heart failure, acute inhibition of angiotensin-converting enzyme with captopril results in falls in both plasma hBNP-li (10% fall) and ANP-li (32% fall) levels. Our results do not support a major role for angiotensin-converting enzyme in the metabolism of human brain natriuretic peptide in heart failure, although a minor role cannot be excluded since the fall in the plasma ANP-li level was greater than the fall in the plasma hBNP-li level. However, the fall in the plasma hBNP-li level is most probably related to the changes induced in intra-cardiac volume/pressure by the angiotensin-converting enzyme inhibitor.