Department of Cardiology, Onze Lieve Vrouwe Ziekenhuis, Moorselbaan 164, B-9300, Aalst, Belgium.
Biomark Med. 2010 Apr;4(2):315-20. doi: 10.2217/bmm.10.5.
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.
成熟的、具有生物学活性的 32 个氨基酸长的 B 型利钠肽（BNP(1-32)）可被心钠肽前体酶（corin）从 BNP 前体中切割产生。最近的数据表明，BNP(1-32)可能是内源性氨基肽酶，二肽基肽酶（DPP）IV 的理想底物。DPP IV 从 BNP(1-32)上切除两个氨基末端氨基酸（Ser 和 Pro），产生 BNP(3-32)，已在心力衰竭患者的血浆中检测到。在犬模型中，与静脉输注 BNP(1-32)相比，静脉输注 BNP(3-32)导致的钠排泄、利尿和血管扩张作用减弱。这些观察结果的临床相关性可能对高血浆 BNP 浓度的患者很重要，因为商业上可获得的免疫测定法可以测量这些浓度。需要进一步的研究来探讨 DPP IV 抑制剂是否可以增加 BNP(1-32)的生物利用度，是否可以延缓心力衰竭的进展，并增加失代偿性心力衰竭中外源性给予 BNP(1-32)的疗效。
