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
Ensembl
UniProt
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[3][4]
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.[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]

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]

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000120937Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000029019Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ Potter LR, Yoder AR, Flora DR, Antos LK, Dickey DM (2009). Natriuretic peptides: their structures, receptors, physiologic functions and therapeutic applications. Handbook of Experimental Pharmacology. Vol. 191. pp. 341–66. doi:10.1007/978-3-540-68964-5_15. ISBN 978-3-540-68960-7. PMC 4855512. PMID 19089336.
  6. ^ Potter LR, Yoder AR, Flora DR, Antos LK, Dickey DM (2009). "Natriuretic Peptides: Their Structures, Receptors, Physiologic Functions and Therapeutic Applications". CGMP: Generators, Effectors and Therapeutic Implications. Handbook of Experimental Pharmacology. Vol. 191. pp. 341–366. doi:10.1007/978-3-540-68964-5_15. ISBN 978-3-540-68960-7. ISSN 0171-2004. PMC 4855512. PMID 19089336.
  7. ^ Potter LR (2009). "Natriuretic peptides: their structures, receptors, physiologic functions and therapeutic applications". Handb Exp Pharmacol (191): 341–66.
  8. ^ "CV Pharmacology - Natriuretic Peptides". cvpharmacology.com. Archived from the original on 21 October 2017. Retrieved 29 April 2018.