BNP Interpretation

Brain natriuretic peptide (BNP) and its inactive N-terminal fragment (NT-proBNP) are neurohormonal biomarkers secreted by ventricular cardiomyocytes in response to myocardial wall stress from volume overload or pressure overload. Understanding the synthesis, release, clearance, and clinical significance of these biomarkers is essential for the NP in diagnosing and managing heart failure. Synthesis and release: When ventricular cardiomyocytes are stretched (increased wall stress from volume or pressure overload), the proBNP gene is activated, producing a 108-amino acid prohormone (proBNP). The enzyme corin (a serine protease on the cardiomyocyte surface) cleaves proBNP into two fragments: the biologically active BNP (32 amino acids, C-terminal fragment) and the inactive NT-proBNP (76 amino acids, N-terminal fragment). Both are released into the circulation proportionally. Physiological actions of BNP: BNP binds to natriuretic peptide receptor A (NPR-A), activating guanylyl cyclase and increasing intracellular cGMP. This produces: natriuresis and diuresis (antagonizing sodium and water retention by RAAS and ADH), vasodilation (reducing preload and afterload), suppression of RAAS (inhibiting renin and aldosterone secretion), inhibition of sympathetic nervous system activation, and antifibrotic/antihypertrophic effects on the myocardium. Essentially, BNP is the...