Why the study?
The clinical relevance of BNP(1-32) cleavage by DPP IV and its impact on heart failure progression and treatment efficacy is not well understood.
Does intravenous BNP(3-32) infusion reduce natriuresis, diuresis and vasodilation compared to BNP(1-32) in a canine model?
Does intravenous BNP(3-32) infusion reduce natriuresis, diuresis and vasodilation compared to BNP(1-32) in a canine model?
BNP(3-32), a cleavage product of BNP(1-32) by DPP IV, has reduced biological activity, suggesting DPP IV inhibitors could potentially increase the bioavailability and efficacy of active BNP in heart failure.
The mature, biologically active 32-amino acid long B-type natriuretic peptide (BNP(1-32)), is cleaved by corin from the BNP prohormone. Recent data demonstrated that BNP(1-32) might be an ideal substrate for the endogenous aminopeptidase, dipeptidyl-peptidase (DPP) IV. DPP IV removes the two amino-terminal amino acids (Ser and Pro) from BNP(1-32) to produce BNP(3-32), which has been detected in plasma of patients with heart failure. In a canine model, intravenous BNP(3-32) infusion resulted in less natriuresis, diuresis and vasodilation compared to intravenous infusion of BNP(1-32). The clinical relevance of these observations may be important for patients with high plasma BNP concentrations, which can be measured by commercially available immunoassays. Further studies are needed to explore whether DPP IV inhibitors increase the bioavailability of BNP(1-32), delay the progression of heart failure and increase the efficacy of exogenously administered BNP(1-32) in decompensated heart failure.
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Vanderheyden et al. (2010) conducted a review in Heart failure. BNP(3-32) vs. BNP(1-32) was evaluated.
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