The natriuretic peptide family includes two major peptides that are secreted by myocardial cells: A-type (ANP) and B-type natriuretic peptide (BNP). While ANP is stored in both atria and ventricles, the major source of BNP are the ventricles (1). Both are synthesized as precursors; BNP is synthesized as pro-BNP in ventricular myocytes, and pro-BNP cleavage leads to two secreted fragments: BNP (32 amino acids [aa]) and N-terminal pro-BNP (NT-pro-BNP) (76 aa). B-type natriuretic peptide is an active hormone with cyclic guanosine monophosphate (cGMP)-mediated vasodilator and natriuretic properties, as well as ANP, and is eliminated by the neutral endopeptidase. Nterminal pro-BNP is mainly eliminated through kidneys and biologically inactive. The half-life of BNP and NT-pro-BNP are 20 and 120 minutes, respectively. Natriuretic peptides blood levels reflect the severity of cardiac diseases and, further, the decompensated state of cardiac dysfunction. Indeed, the main stimulus of the constitutive pro-BNP synthesis is the mechanical strain within the ventricular wall, which depends on ventricular mass, geometry, and diastolic pressures. © 2008 Springer-Verlag London.
CITATION STYLE
Logeart, D., & Solal, A. C. (2008). B-type natriuretic peptide testing in the emergency room and intensive care unit for the patient with acute heart failure. In Acute Heart Failure (pp. 468–474). Springer London. https://doi.org/10.1007/978-1-84628-782-4_43
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