THE FAMILY of natriuretic peptides, which includes atrial natriuretic peptide (ANP), B-type
natriuretic peptide (BNP), and C-type natriuretic peptide (CNP), has a
regulatory and modulatory role in the cardiovascular
system.1,2 ANP and BNP are circulating cardiac hormones.
ANP is synthesized by myocytes mainly in the atria and stored in
granules. BNP, also known as brain natriuretic peptide because it was
first isolated from porcine brain, is synthesized primarily by cardiac
myocytes in the ventricles and is not stored to the same extent as ANP.
The nucleic acid sequence of the BNP gene contains the destabilizing
sequence TATTTAT, which suggests that the turnover of BNP messenger RNA
(mRNA) is high and that BNP is synthesized in bursts. In response to
stretching of the right atrium by increased venous pressure, stored ANP
is immediately released from atrial granules, whereas an increase in
BNP secretion is preceded by an increase in mRNA.3 Thus,
intravenous saline loading increases plasma ANP acutely, but there is
no corresponding immediate increase in plasma BNP.4 In
contrast, the increase in intravascular volume from dietary salt
loading results in the expected increase in BNP.4
Similarly, a change in a patient's pacemaker mode from atrial to
ventricular pacing leading to uncoordinated atrial contractions and
high pressure waves causes a greater acute increase in plasma ANP than
BNP.5 It therefore appears that BNP level reflects
long-term intravascular volume status rather than momentary volume.
Moreover, BNP is more stable than ANP in plasma and has a longer
half-life,6 which may be attributable to its lesser
affinity for clearance receptors. CNP is synthesized in the endothelium
and has vasodilatory and antiproliferative effects on vascular smooth
muscle. It has a local action in the blood vessels or within the organ
where it is produced.
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