Brain natriuretic peptide 32

NPPB
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesNPPB, natriuretic peptide B, BNP, Iso-ANP, ventricular natriuretic peptide
External IDsOMIM: 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 MbChr 4: 148.07 – 148.07 Mb
PubMed search
Wikidata
View/Edit HumanView/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. BNP is one of the three natriuretic peptides, in addition to atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP). 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.

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.