Cardiac hormone that plays a key role in mediating cardio-renal homeostasis (By similarity). May also function as a paracrine antifibrotic factor in the heart (By similarity). Acts by specifically binding and stimulating NPR1 to produce cGMP, which in turn activates effector proteins that drive various biological responses. Involved in regulating the extracellular fluid volume and maintaining the fluid-electrolyte balance through natriuresis, diuresis, vasorelaxation, and inhibition of renin and aldosterone secretion. Binds the clearance receptor NPR3 (By similarity). Plays a key role in cardiovascular homeostasis through natriuresis, diuresis, vasorelaxation, and inhibition of renin and aldosterone secretion (PubMed:2964562). In vivo, induces vasodilation (PubMed:2964562). May affect cardio-renal homeostasis. Able to promote the production of cGMP although its potency is very low compared to brain natriuretic peptide 32. Detected in blood. Detected in blood. Heart atrium. Brain (at protein level). Brain (at protein level). The precursor molecule is proteolytically cleaved by the endoproteases FURIN or CORIN at Arg-99 to produce the active brain natriuretic peptide 32 and the inactive NT-proBNP. CORIN also cleaves the precursor molecule at additional residues including Arg-96 and possibly Lys-102 (By similarity). Undergoes further proteolytic cleavage by unknown proteases to give rise to Brain natriuretic peptide 26 (PubMed:3421965). Undergoes further proteolytic cleavage by various proteases such as DPP4, MME and possibly FAP, to give rise to a variety of shorter peptides. Cleaved at Pro-101 by the prolyl endopeptidase FAP (seprase) activity (in vitro). Degraded by IDE. During IDE degradation, the resulting products initially increase the activation of NPR1 and can also stimulate NPR2 to produce cGMP before the fragments are completely degraded and inactivated by IDE (in vitro). Belongs to the natriuretic peptide family.