SummaryBecause both atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) competitively bind to natriuretic peptide receptors but not N-terminal proBNP (NT-proB-NP), the diagnostic value of BNP as a marker of the severity of heart failure in comparison with NT-proBNP during exogenous ANP (carperitide) infusion remains unclear.Forty-two patients with CHF (NYHA class III or IV) treated with the infusion of carperitide were included in the present study. We measured plasma levels of BNP and NT-proBNP at baseline and after the improvement of symptoms. We also measured these parameters before and 1 hour after stopping the infusion of carperitide.After stopping the infusion of carperitide, the plasma BNP level was significantly decreased by about 20% (394 ± 53.8 versus 312.8 ± 46 pg/mL, P < 0.0001) but plasma NT-proBNP did not change (1674.5 ± 282.1 versus 1777.5 ± 300.3 pg/mL, P = 0.259). The molar ratio of plasma BNP/NT-proBNP was significantly higher during carperitide infusion (0.74 ± 0.08) than those at baseline (0.63 ± 0.06) and after stopping carperitide (0.59 ± 0.07).During carperitide infusion, plasma NT-proBNP may be a more reliable marker of endogenous cardiac natriuretic peptides than plasmaBNP, which may be increased by carperitide infusion. (Int Heart J 2009; 50: 183-190) Key words: Atrial natriuretic peptide, Brain natriuretic peptide, NT-proBNP, Carperitide BRAIN or B-type natriuretic peptide (BNP) is synthesized as preproBNP mainly in the ventricular myocardium. During ventricular myocyte stretching, preproBNP is enzymatically cleaved to proBNP and released in the form of hormonally active BNP and inactive NT-proBNP. Atrial natriuretic peptide (ANP) and BNP have biologic effects such as natriuresis, diuresis, vasodilatation, and From the