Natriuretic peptides B (BNP)

Natriuretic peptides B, commonly known as Brain Natriuretic Peptide (BNP), is a 32-amino acid peptide hormone primarily synthesized and secreted by the ventricular myocardium in response to increased wall tension and volume expansion [4, 8, 9]. It serves as a key regulator of cardiovascular and renal homeostasis by promoting natriuresis, diuresis, and systemic vasodilation, while simultaneously antagonizing the effects of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system [1, 4, 16]. BNP exerts its biological actions by binding to the natriuretic peptide receptor A (NPR-A), which stimulates membrane-bound guanylyl cyclase to increase intracellular levels of cyclic guanosine monophosphate (cGMP) [1, 7, 14]. In clinical medicine, plasma levels of BNP and its inactive N-terminal pro-hormone fragment (NT-proBNP) are widely utilized as essential diagnostic and prognostic biomarkers for heart failure and other cardiovascular conditions [6, 9, 17]. Therapeutic strategies involving this target include the administration of recombinant BNP (nesiritide) for acute decompensated heart failure and the use of neprilysin inhibitors (e.g., sacubitril) to prevent the enzymatic degradation of endogenous natriuretic peptides, thereby enhancing their beneficial hemodynamic effects [9, 12, 20].

Other names

Brain natriuretic peptideB-type natriuretic peptideNPPBproBNPNT-proBNPGamma-brain natriuretic peptideBrain natriuretic peptide 32

Agonism of Natriuretic peptide receptor 1 (NPR1/NPR-A) to increase intracellular cGMP; Inhibition of enzymatic degradation by neprilysin to increase endogenous peptide levels.