Brain natriuretic peptide 32

Last updated

NPPB
Available structures
PDB Ortholog search: PDBe RCSB
Identifiers
Aliases NPPB , natriuretic peptide B, BNP, Iso-ANP, ventricular natriuretic peptide
External IDs OMIM: 600295; MGI: 97368; HomoloGene: 81698; GeneCards: NPPB; OMA:NPPB - orthologs
Orthologs
SpeciesHumanMouse
Entrez

4879

18158

Ensembl

ENSG00000120937

ENSMUSG00000029019

UniProt

P16860

P40753

RefSeq (mRNA)

NM_002521

NM_001287348
NM_008726

RefSeq (protein)

NP_002512
NP_002512

NP_001274277
NP_032752

Location (UCSC) Chr 1: 11.86 – 11.86 Mb Chr 4: 148.07 – 148.07 Mb
PubMed search [3] [4]
Wikidata
View/Edit Human View/Edit Mouse

Brain natriuretic peptide (BNP), also known as B-type natriuretic peptide, is a hormone secreted by cardiomyocytes in the heart ventricles in response to stretching caused by increased ventricular blood volume. [5] BNP is one of the three natriuretic peptides, in addition to atrial natriuretic peptide (ANP) and C-type natriuretic peptide ( CNP). [6] BNP was first discovered in porcine brain tissue in 1988, which led to its initial naming as "brain natriuretic peptide", although subsequent research revealed that BNP is primarily produced and secreted by the ventricular myocardium (heart muscle) in response to increased ventricular blood volume and stretching. To reflect its true source, BNP is now often referred to as "B-type natriuretic peptide" while retaining the same acronym. [7]

Contents

The 32-amino acid polypeptide BNP-32 is secreted attached to a 76–amino acid N-terminal fragment in the prohormone called NT-proBNP (BNPT), which is biologically inactive. Once released, BNP binds to and activates the atrial natriuretic factor receptor NPRA, and to a lesser extent NPRB, in a fashion similar to atrial natriuretic peptide (ANP) but with 10-fold lower affinity. The biological half-life of BNP, however, is twice as long as that of ANP, and that of NT-proBNP is even longer, making these peptides better targets than ANP for diagnostic blood testing.

The physiologic actions of BNP are similar to those of ANP and include decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis. The net effect of these peptides is a decrease in blood pressure due to the decrease in systemic vascular resistance and, thus, afterload. Additionally, the actions of both BNP and ANP result in a decrease in cardiac output due to an overall decrease in central venous pressure and preload as a result of the reduction in blood volume that follows natriuresis and diuresis. [8]

Biosynthesis

BNP is synthesized as a 134-amino acid preprohormone (preproBNP), encoded by the human gene NPPB. Removal of the 26-residue N-terminal signal peptide generates the prohormone, proBNP, which is stored intracellularly as an O-linked glycoprotein; proBNP is subsequently cleaved between arginine-102 and serine-103 by a specific convertase (probably furin or corin) into NT-proBNP and the biologically active 32-amino acid polypeptide BNP-32, which are secreted into the blood in equimolar amounts. [9] [10] Cleavage at other sites produces shorter BNP peptides with unknown biological activity. [11] Processing of proBNP may be regulated by O-glycosylation of residues near the cleavage sites. [12] The synthesis of BNP in cardiomyocytes is stimulated by pro-inflammatory cell factors, such as interleukin-1β, interleukin-6 and tumor necrosis factor-α. [13]

Physiologic effects

Renal

Adrenal

Vascular

Relaxes vascular smooth muscle in arterioles and venules by:

Promotes uterine spiral artery remodeling, which is important for preventing pregnancy-induced hypertension. [16]

Cardiac

Adipose tissue

Measurement

BNP and NT-proBNP are measured by immunoassay. [18]

Interpretation of BNP

A preoperative BNP can be predictive of a risk of an acute cardiac event during vascular surgery. A cutoff of 100 pg/ml has a sensitivity of approximately 100%, a negative predictive value of approximately 100%, a specificity of 90%, and a positive predictive value of 78% according to data from the United Kingdom. [23]

BNP is cleared by binding to natriuretic peptide receptors (NPRs) and neutral endopeptidase (NEP). Less than 5% of BNP is cleared renally. NT-proBNP is the inactive molecule resulting from cleavage of the prohormone Pro-BNP and is reliant solely on the kidney for excretion. The achilles heel of the NT-proBNP molecule is the overlap in kidney disease in the heart failure patient population. [24] [25]

Some laboratories report in units ng per Litre (ng/L), which is equivalent to pg/mL

There is a diagnostic 'gray area', often defined as between 100 and 500 pg/mL, for which the test is considered inconclusive, but, in general, levels above 500 pg/ml are considered to be an indicator of heart failure. This so-called gray zone has been addressed in several studies, and using clinical history or other available simple tools can help make the diagnosis. [26] [27]

BNP has been suggested as a predictor for a variety of medical states, including cardiovascular mortality in diabetics [28] and cardiac impairment in cancer patients. [29] [30]

BNP was found to have an important role in prognostication of heart surgery patients [31] and in the emergency department. [32] It has been shown that combining BNP with other tools like impedance cardiography (ICG) can improve early diagnosis of heart failure and advance prevention strategies. [33] [34] Utility of BNP has also been explored in various settings like preeclampsia, intensive care, shock and end-stage renal disease (ESRD). [35] [36] [37]

The effect or race and gender on value of BNP and its utility in that context has been studied extensively. [38] [39]

NT-proBNP levels (in pg/mL) by New York Heart Association Functional Classification (NYHA functional class) [40]
NYHA INYHA IINYHA IIINYHA IV
5th Percentile33103126148
Mean1015166630293465
95th Percentile3410656710,44912,188

The BNP test is used as an aid in the diagnosis and assessment of severity of heart failure. A recent meta-analysis concerning effects of BNP testing on clinical outcomes of patients presenting to the emergency department with acute dyspnea revealed that BNP testing led to a decrease in admission rates and decrease in mean length of stay, although neither was statistically significant. Effects on all cause hospital mortality was inconclusive. [41] The BNP test is also used for the risk stratification of patients with acute coronary syndromes. [42] [43]

When interpreting an elevated BNP level, values may be elevated due to factors other than heart failure. Lower levels are often seen in obese patients. [44] Higher levels are seen in those with renal disease, in the absence of heart failure.

Therapeutic application

Recombinant BNP, nesiritide, has been suggested as a treatment for decompensated heart failure. However, a clinical trial failed to show a benefit of nesiritide in patients with acute decompensated heart failure. [45] Blockade of neprilysin, a protease known to degrade members of the natriuretic peptide family, has also been suggested as a possible treatment for heart failure. Dual administration of neprilysin inhibitors and angiotensin receptor blockers has been shown to be advantageous to ACE inhibitors, the current first-line therapy, in multiple settings. [46] [47]

See also

Related Research Articles

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<span class="mw-page-title-main">Atrial natriuretic peptide</span> Cardiac hormone which increases renal sodium excretion

Atrial natriuretic peptide (ANP) or atrial natriuretic factor (ANF) is a natriuretic peptide hormone secreted from the cardiac atria that in humans is encoded by the NPPA gene. Natriuretic peptides are a family of hormone/paracrine factors that are structurally related. The main function of ANP is causing a reduction in expanded extracellular fluid (ECF) volume by increasing renal sodium excretion. ANP is synthesized and secreted by cardiac muscle cells in the walls of the atria in the heart. These cells contain volume receptors which respond to increased stretching of the atrial wall due to increased atrial blood volume.

Hypertrophic cardiomyopathy is a condition in which muscle tissues of the heart become thickened without an obvious cause. The parts of the heart most commonly affected are the interventricular septum and the ventricles. This results in the heart being less able to pump blood effectively and also may cause electrical conduction problems. Specifically, within the bundle branches that conduct impulses through the interventricular septum and into the Purkinje fibers, as these are responsible for the depolarization of contractile cells of both ventricles.

<span class="mw-page-title-main">Atrium (heart)</span> Part of the human heart

The atrium is one of the two upper chambers in the heart that receives blood from the circulatory system. The blood in the atria is pumped into the heart ventricles through the atrioventricular mitral and tricuspid heart valves.

Tachycardia-induced cardiomyopathy (TIC) is a disease where prolonged tachycardia or arrhythmia causes an impairment of the myocardium, which can result in heart failure. People with TIC may have symptoms associated with heart failure and/or symptoms related to the tachycardia or arrhythmia. Though atrial fibrillation is the most common cause of TIC, several tachycardias and arrhythmias have been associated with the disease.

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<span class="mw-page-title-main">Cardiac amyloidosis</span> Medical condition

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<span class="mw-page-title-main">Natriuretic peptide</span> Hormone used in regulating the cardiovascular system

A natriuretic peptide is a hormone molecule that plays a crucial role in the regulation of the cardiovascular system. These hormones were first discovered in the 1980s and were found to have very strong diuretic, natriuretic, and vasodilatory effects. There are three main types of natriuretic peptides: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). Two minor hormones include urodilatin (URO) which is processed in the kidney and encoded by the same gene as ANP, and dendroaspis NP (DNP) that was discovered through isolation of the venom from the green mamba snake. Since they are activated during heart failure, they are important for the protection of the heart and its tissues.

<span class="mw-page-title-main">Natriuretic peptide precursor C</span> Protein-coding gene in the species Homo sapiens

Natriuretic peptide precursor C, also known as NPPC, is a protein that in humans is encoded by the NPPC gene. The precursor NPPC protein is cleaved to the 22 amino acid peptide C-type natriuretic peptide (CNP).

<span class="mw-page-title-main">NPR2</span> Human protein-coding gene

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<span class="mw-page-title-main">NPR3</span> Protein-coding gene in humans

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<span class="mw-page-title-main">CORIN</span> Mammalian protein found in Homo sapiens

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References

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  39. ↑ Daniels LB, Bhalla V, Clopton P, Hollander JE, Guss D, McCullough PA, et al. (May 2006). "B-type natriuretic peptide (BNP) levels and ethnic disparities in perceived severity of heart failure: results from the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT) multicenter study of BNP levels and emergency department decision making in patients presenting with shortness of breath". Journal of Cardiac Failure. 12 (4): 281–5. doi:10.1016/j.cardfail.2006.01.008. PMID   16679261.
  40. ↑ "N-terminal-pro-BNP". LABORATORY SERVICES HANDBOOK. The University of Iowa (UIHC), Department of Pathology. 28 May 2020. Archived from the original on 2008-10-11. Showing 95th percentiles. Epic Lab Code: LAB649.
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  45. ↑ O'Connor CM, Starling RC, Hernandez AF, Armstrong PW, Dickstein K, Hasselblad V, et al. (July 2011). "Effect of nesiritide in patients with acute decompensated heart failure" (PDF). The New England Journal of Medicine. 365 (1): 32–43. doi:10.1056/NEJMoa1100171. hdl: 11379/60663 . PMID   21732835.
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Further reading

attribution: copied from Brain natriuretic peptide version as of 13:57, 4 December 2019

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