Abstract
As a family of hormones with pleiotropic effects, natriuretic peptide (NP) system includes atrial NP (ANP), B-type NP (BNP), C-type NP (CNP), dendroaspis NP and urodilatin, with NP receptor-A (guanylate cyclase-A), NP receptor-B (guanylate cyclase-B) and NP receptor-C (clearance receptor). These peptides are genetically distinct, but structurally and functionally related for regulating circulatory homeostasis in vertebrates. In humans, ANP and BNP are encoded by NP precursor A (NPPA) and NPPB genes on chromosome 1, whereas CNP is encoded by NPPC on chromosome 2. NPs are synthesized and secreted through certain mechanisms by cardiomyocytes, fibroblasts, endotheliocytes, immune cells (neutrophils, T-cells and macrophages) and immature cells (embryonic stem cells, muscle satellite cells and cardiac precursor cells). They are mainly produced by cardiovascular, brain and renal tissues in response to wall stretch and other causes. NPs provide natriuresis, diuresis, vasodilation, antiproliferation, antihypertrophy, antifibrosis and other cardiometabolic protection. NPs represent body’s own antihypertensive system, and provide compensatory protection to counterbalance vasoconstrictor-mitogenic-sodium retaining hormones, released by renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS). NPs play central roles in regulation of heart failure (HF), and are inactivated through not only NP receptor-C, but also neutral endopeptidase (NEP), dipeptidyl peptidase-4 and insulin degrading enzyme. Both BNP and N-terminal proBNP are useful biomarkers to not only make the diagnosis and assess the severity of HF, but also guide the therapy and predict the prognosis in patients with HF. Current NP-augmenting strategies include the synthesis of NPs or agonists to increase NP bioactivity and inhibition of NEP to reduce NP breakdown. Nesiritide has been established as an available therapy, and angiotensin receptor blocker NEP inhibitor (ARNI, LCZ696) has obtained extremely encouraging results with decreased morbidity and mortality. Novel pharmacological approaches based on NPs may promote a therapeutic shift from suppressing the RAAS and SNS to re-balancing neuroendocrine dysregulation in patients with HF. The current review discussed the synthesis, secretion, function and metabolism of NPs, and their diagnostic, therapeutic and prognostic values in HF.
Highlights
As a family of hormones with pleiotropic effects, natriuretic peptide (NP) system includes atrial NP (ANP), Btype NP (BNP, called brain NP), C-type NP (CNP), dendroaspis NP (DNP) and urodilatin, with three receptors: NP receptor-A [guanylate cyclase (GC)-A or NPRA], NP receptor-B (GC-B or Natriuretic peptide receptor (NPR)-B) and NP receptor-C [1]
As a family of hormones with pleiotropic effects, natriuretic peptide (NP) system includes atrial NP (ANP), Btype NP (BNP, called brain NP), C-type NP (CNP), dendroaspis NP (DNP) and urodilatin, with three receptors: NP receptor-A [guanylate cyclase (GC)-A or NPRA], NP receptor-B (GC-B or NPR-B) and NP receptor-C [1]. These peptides are genetically distinct, but structurally and functionally related for regulating circulatory homeostasis in vertebrates, and each of them has a 17-amino acid cyclic structure constructed with an disulfide bond [2]
ANP and B-type NP (BNP) are encoded by NP precursor A (NPPA) and NPPB genes on chromosome 1, whereas CNP is encoded by NPPC on chromosome 2 [3]
Summary
As a family of hormones with pleiotropic effects, natriuretic peptide (NP) system includes atrial NP (ANP), Btype NP (BNP, called brain NP), C-type NP (CNP), dendroaspis NP (DNP) and urodilatin, with three receptors: NP receptor-A [guanylate cyclase (GC)-A or NPRA], NP receptor-B (GC-B or NPR-B) and NP receptor-C (clearance receptor or NPR-C) [1]. NPs are synthesized and secreted through certain mechanisms by cardiomyocytes, fibroblasts, endotheliocytes, immune cells (neutrophils, T-cells and macrophages) and immature cells, such as embryonic stem cells, muscle satellite cells and cardiac precursor cells (CPCs) [4]. They are mainly produced by cardiovascular, brain and renal tissues in response to wall stretch and other causes. The current review discussed the synthesis, secretion, function and metabolism of NPs, and their diagnostic, therapeutic and prognostic values in heart failure (HF)
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