BNP – a peptide about cardiovascular and cerebrovascular diseases

Brain natriuretic peptide (BNP), now known as B-type natriuretic peptide or Ventricular Natriuretic Peptide (still BNP), is a 32-amino acid polypeptide secreted by the ventricles of the heart in response to excessive stretching of heart muscle cells (cardiomyocytes). The release of BNP is modulated by calcium ions.[1] BNP is named as such because it was originally identified in extracts of porcine brain, although in humans it is produced mainly in the cardiac ventricles.

BNP is secreted along with a 76-amino acid N-terminal fragment (NT-proBNP) that is biologically inactive. BNP binds to and activates the atrial natriuretic factor receptors 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. Thus, the net effect of BNP and ANP is a decrease in blood volume, which lowers systemic blood pressure and afterload, yielding an increase in cardiac output, partly due to a higher ejection fraction.

BNP is synthesized as a 134-amino acid preprohormone (preproBNP), encoded by the human gene NPPB. Removal of the 25-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.[2] Cleavage at other sites produces shorter BNP peptides with unknown biological activity.[3] Processing of proBNP may be regulated by O-glycosylation of residues near the cleavage sites.

The main clinical utility of either BNP or NT-proBNP is that a normal level rules out acute heart failure in the emergency setting. An elevated BNP or NT-proBNP should never be used to “rule in” acute or heart failure in the emergency setting due to lack of specificity. [3] It appears to have become a common misconception in many emergency departments that ordering brain natriuretic peptide studies in a routine manner has reliable positive predictive value (PPV). However, the value of the test in terms of PPV has simply not been shown. Using these studies inappropriately in such a way would likely result in increased healthcare costs, however an extensive study regarding the potential cost has yet to be performed.

BNP can be elevated in renal failure. 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.

Recombinant BNP, nesiritide, is used to treat decompensated heart failure. However, a recent clinical trial failed to show a benefit of nesiritide in patients with acute decompensated heart failure, and the authors could not recommend its use.

Karebay can synthetic BNP with Cyanine or other fluorescent moleculars , so that scientists can knew more details about its molecular mechanism.

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Reference [1] Ziskoven D, Forssmann WG, Holthausen U, et al. (1989). “Calcium Calmodulin antagonists Influences the release of Cardiodilatin/ANP from Atrial Cardiocytes”. In Kaufmann W, Wambach G. Handbook Endocrinology of the Heart. Berlin: Verlag: Springer. pp. 233–4. [2] Schellenberger U, O’Rear J, Guzzetta A,et al. (July 2006). “The precursor to B-type natriuretic peptide is an O-linked glycoprotein”. Arch. Biochem. Biophys. 451 (2): 160–6. [3] Niederkofler EE, Kiernan UA, O’Rear J,et al.(November 2008). “Detection of endogenous B-type natriuretic peptide at very low concentrations in patients with heart failure”. Circ Heart Fail 1 (4): 258–64.

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