Brain natriuretic peptide (BNP)(also known as B-type natriuretic peptide or "GC-B") is a 32 amino acid polypeptide secreted by the ventricles of the heart in response to excessive stretching of myocytes (heart muscles cells) in the ventricles.  At the time of release, a co-secreted 76 amino acid N-terminal fragment (NT-proBNP) is also released with BNP. BNP binds to and activates NPRA in a similar fashion 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. Both ANP and BNP have limited ability to bind and activate NPRB.

Brain natriuretic peptide was originally identified in extracts of porcine brain, but in humans it is produced mainly in the cardiac ventricles. Physiologic actions of BNP and ANP include decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis. Thus, the resulting effect of these peptides is a decrease in cardiac output and a decrease in blood volume.

Tests showing elevated levels of BNP or NT-proBNP in the blood are used as a diagnosis of heart failure and may be useful to establish prognosis in heart failure, as both markers are typically higher in patients with worse outcome.  Both BNP and NT-proBNP have been approved as a marker for acute congestive heart failure (CHF). The plasma concentrations of both BNP are increased in patients with asymptomatic and symptomatic left ventricular dysfunction.

There is no level of BNP that perfectly separates patients with and without heart failure. For patients with CHF, values will generally be above 100 pg per milliliter; however, a more conservative interpretation of the BNP is that normal values are less than 50 pg per milliliter in order to achieve adequate sensitivity. There is a diagnostic 'gray area', often defined as between 100 and 500, for which the test is considered inconclusive. Values above 500 are generally considered to be positive.