What is the normal activity of brain natriuretic peptide (BNP)?

Updated: Jan 08, 2018
  • Author: Donald Schreiber, MD, CM; Chief Editor: Erik D Schraga, MD  more...
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Brain natriuretic peptide (BNP) is a member of a family of four human natriuretic peptides that share a common 17-peptide ring structure. [1] The first was identified in 1983 and named atrial natriuretic peptide (ANP). ANP is a 28-amino acid polypeptide resulting from the C-terminal end of the prohormone proANP. The source is largely in the cardiac atria, and ANP is quickly secreted in response to atrial stretching. Normal hearts secrete extremely small amounts of ANP, but elevated levels are found in patients with left ventricular (LV) hypertrophy and mitral valve disease.

A closely related molecule was first identified in pig brains in 1988 and therefore named BNP. However, BNP was subsequently discovered to be present in high concentrations in cardiac tissues, particularly the ventricles. Two additional natriuretic peptides, designated C-type natriuretic peptide (CNP) and Dendroaspis natriuretic peptide (DNP), have also been described; they are thought to act in the peripheral vasculature and the atria, respectively.

Before its activation, BNP is stored as a 108–amino acid polypeptide precursor, proBNP, in secretory granules in both ventricles and, to a lesser extent, in the atria. After proBNP is secreted in response to volume overload and resulting myocardial stretch, it is cleaved to the 76-peptide, biologically inert N -terminal fragment NT-proBNP and the 32-peptide, biologically active hormone BNP. The 2 fragments are secreted into the plasma in equimolar amounts, and both have been clinically evaluated for use in the management of congestive heart failure (CHF).

High ventricular filling pressures stimulate the release of ANP and BNP. Both peptides have diuretic, natriuretic, and antihypertensive effects, which they exert by inhibiting the renin-angiotensin-aldosterone system. They also have systemic and renal sympathetic activity. In addition, BNP may provide a protective effect against the detrimental fibrosis and remodeling that occurs in progressive heart failure.

Although ANP was identified first, concentrations of BNP in the myocardial tissue were found to be higher than those of ANP. Therefore, BNP has been studied more intensely than ANP as a clinically useful marker of increased ventricular filling pressure. An elevated BNP level is a marker of increased LV filling pressures and LV dysfunction.

Natriuretic peptide receptors and plasma endopeptidases actively clear BNP from the circulation; the plasma half-life is thus short, approximately 20 minutes. No receptor-mediated clearance of NT-proBNP is known to occur, and NT-proBNP has a correspondingly prolonged half-life of 60-120 minutes. As a result, plasma levels of NT-proBNP tend to be 3-5 times higher than BNP levels. Clearance of NT-proBNP is thought to be primarily renal. Therefore, the renal clearance of NT-proBNP confounds its diagnostic utility in patients with renal insufficiency.

As a laboratory specimen, NT-proBNP is more stable during storage than BNP. NT-proBNP samples are stable at room temperature for 72 hours, versus less than 4 hours for BNP samples.

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