RT Journal
A1 Piña IL, O’Connor C
T1 BNp-guided therapy for heart failure
JF JAMA
JO JAMA
YR 2009
FD January 28
VO 301
IS 4
SP 432
OP 434
DO 10.1001/jama.2009.3
UL http://dx.doi.org/10.1001/jama.2009.3
AB 
The current status of BNP in heart failure has been the result of an important historic journey. In 1981, de Bold et al1 injected myocardial homogenates into nondiuretic rats. The atrial muscle extract increased sodium and chloride excretion 30-fold, along with an impressive increase in urine volume. By 1985, this same group had identified specific granules that secreted the peptide, now known as atrial natriuretic factor (ANF), and noted that the substance also had a hypotensive effect and an inhibitory action on renin and aldosterone secretion.2 Thus, the heart was behaving as an endocrine organ. The investigators noted that the inability of the kidney to excrete sodium in chronic heart failure could be related to ANF and that the peptide might hold promise in the therapy for both hypertension and heart failure. Francis et al3 subsequently described the elevation of ANF early in heart failure and surprisingly in patients with asymptomatic left ventricular dysfunction. Several years later in 1988, Sudoh et al,4 from Japan, isolated an ANF-like peptide from mammalian brain tissue that had similar properties to ANF but was distinct in its amino acid sequence, hence the name brain natriuretic peptide. These investigators suggested that in human disease, both ANF and BNP might perhaps have a dual mechanistic action in sodium and volume homeostasis.