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Brain Natriuretic Peptide, Human

CAT#
10-101-25
Synonyms/Alias
Natriuretic Peptide, Brain; BNP-32; Natrecor; BNP; B-Type Natriuretic Peptide; BNP32; BNP 32; Nesiritide; Type-B Natriuretic Peptide
CAS No.
124584-08-3 (net)
Sequence
H-Ser-Pro-Lys-Met-Val-Gln-Gly-Ser-Gly-Cys-Phe-Gly-Arg-Lys-Met-Asp-Arg-Ile-Ser-Ser-Ser-Ser-Gly-Leu-Gly-Cys-Lys-Val-Leu-Arg-Arg-His-OH Acetate salt (Disulfide bond)
M.W/Mr.
3464.09
Molecular Formula
C143H244N50O42S4
Source
Synthetic
Long-term Storage Conditions
−20°C
Application
Brain natriuretic peptide (BNP) decreases the systemic vascular resistance and central venous pressure as well as increases the natriuresis. Thus, the net effect of BNP and atrial natriuretic peptide (ANP) is a decrease in blood volume, which lowers systemic blood pressure and afterload, yielding an increase in cardiac output, partly due to a higher ejection fraction.
Description
Brain natriuretic peptide, uretic peptide or Ventricular Natriuretic Peptide (still BNP), is a 32-amino acid polypeptide secreted by the ventricles of the heart in response to excessive stretching of heart muscle cells (cardiomyocytes). BNP is named as such because it was originally identified in extracts of porcine brain, although in humans it is produced mainly in the cardiac ventricles.
Areas of Interest
Cardiovascular Therapeutics

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BNP was primarily discovered in porcine brain, but the highest concentration of peptide is found in the heart. It is a 32 amino-acid peptide, synthesized within the ventricles in response to myocyte stretch and/or pressure overload. It is released both as an active hormone and an inactive N-terminal fragment (NT pro-BNP).

Higher BNP concentrations early after first myocardial infarction are associated with adverse left ventricular remodelling characteristics. This may help explain why BNP is such a strong predictor of outcome after myocardial infarction.

Crilley J G, Farrer M. Left ventricular remodelling and brain natriuretic peptide after first myocardial infarction[J]. Heart, 2001, 86(6): 638-642.

Subtle cardiac abnormalities have been described in patients with cirrhosis. Natriuretic peptide hormones have been reported to be sensitive markers of early cardiac disease. We postulate that plasma levels of N-terminal pro-atrial natriuretic peptide and brain natriuretic peptide could be used as markers of cardiac dysfunction in cirrhosis.

Florence W, Samuel S I U, Peter L I U, et al. Brain natriuretic peptide: is it a predictor of cardiomyopathy in cirrhosis?[J]. Clinical Science, 2001, 101(6): 621-628.

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