negative regulation of systemic arterial blood pressure
neuropeptide signaling pathway
cGMP-mediated signaling
regulation of blood pressure
negative regulation of angiogenesis
cell surface receptor signaling pathway
regulation of vascular permeability
receptor guanylyl cyclase signaling pathway
body fluid secretion
antimicrobial humoral immune response mediated by antimicrobial peptide
cGMP biosynthetic process
negative regulation of cell growth
positive regulation of urine volume
positive regulation of renal sodium excretion
Sources:Amigo / QuickGO
Orthologs
Species
Human
Mouse
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 32 (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 ANP and CNP.[6]
The 32-amino acid polypeptide BNP 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.[7]
^ abcGRCh38: Ensembl release 89: ENSG00000120937 – Ensembl, May 2017
^ abcGRCm38: Ensembl release 89: ENSMUSG00000029019 – Ensembl, May 2017
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^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.
^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.
^"CV Pharmacology - Natriuretic Peptides". cvpharmacology.com. Archived from the original on 21 October 2017. Retrieved 29 April 2018.
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Brainnatriureticpeptide32 (BNP), also known as B-type natriureticpeptide, is a hormone secreted by cardiomyocytes in the heart ventricles in response...
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acid peptide C-type natriureticpeptide (CNP). Natriureticpeptides comprise a family of 3 structurally related molecules: atrial natriureticpeptide (ANP)...
failure, according to guidelines published 2018 by NICE in the UK. Brainnatriureticpeptide32 (BNP) is another biomarker commonly tested for heart failure...
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