Reference values for N-terminal pro-B-type natriuretic peptide in umbilical cord blood.

Plasma concentrations of B-type natriuretic peptide (BNP), a 32-amino acid peptide hormone secreted by the myocardium, increase in response to myocardial stretch or strain (1)(2). On secretion, proBNP, the storage form of BNP, is cleaved into the inactive N-terminal proBNP (NT-proBNP) and the endocrinologically active BNP. In patients with heart failure, plasma BNP concentrations are related to the severity of symptoms and underlying cardiac abnormality (3). It is also known that neonates show transient increases in both plasma NT-proBNP and BNP in the first days of life as a result of the increased left ventricular volume load induced by the circulatory changes …

[1]  J. Goetze Biochemistry of pro-B-type natriuretic peptide-derived peptides: the endocrine heart revisited. , 2004, Clinical chemistry.

[2]  A. Korach,et al.  N‐terminal pro‐B‐type natriuretic peptide: reference plasma levels from birth to adolescence. Elevated levels at birth and in infants and children with heart diseases , 2004, Acta paediatrica.

[3]  M. Emdin,et al.  Cardiac natriuretic hormones, neuro-hormones, thyroid hormones and cytokines in normal subjects and patients with heart failure , 2004, Clinical chemistry and laboratory medicine.

[4]  T. Mir,et al.  Plasma concentrations of aminoterminal pro atrial natriuretic peptide and aminoterminal pro brain natriuretic peptide in healthy neonates: marked and rapid increase after birth. , 2003, Pediatrics.

[5]  G. Brandenberger,et al.  Mechanisms of renal hyporesponsiveness to ANP in heart failure , 2003, European journal of clinical investigation.

[6]  J. Rehfeld,et al.  The paradox of increased natriuretic hormones in congestive heart failure patients: does the endocrine heart also fail in heart failure? , 2003, European heart journal.

[7]  V. Cameron,et al.  Minireview: natriuretic peptides during development of the fetal heart and circulation. , 2003, Endocrinology.

[8]  Rehfeld Jf,et al.  The posttranslational phase of gene expression: new possibilities in molecular diagnosis. , 2003 .

[9]  A. Clerico Pathophysiological and Clinical Relevance of Circulating Levels of Cardiac Natriuretic Hormones: Are They Merely Markers of Cardiac Disease? , 2002, Clinical chemistry and laboratory medicine.

[10]  M. Andreassi,et al.  Up‐regulation of ‘clearance’ receptors in patients with chronic heart failure: a possible explanation for the resistance to biological effects of cardiac natriuretic hormones , 2001, European journal of heart failure.

[11]  G. Iervasi,et al.  Turnover studies on cardiac natriuretic peptides: methodological, pathophysiological and therapeutical considerations. , 2000, Current drug metabolism.

[12]  J. Tremblay,et al.  Alteration of lung atrial natriuretic peptide receptors in genetic cardiomyopathy. , 1996, The American journal of physiology.

[13]  V. Cameron,et al.  The sites of gene expression of atrial, brain, and C-type natriuretic peptides in mouse fetal development: temporal changes in embryos and placenta. , 1996, Endocrinology.

[14]  G. Iervasi,et al.  Alterations in metabolic clearance of atrial natriuretic peptides in heart failure: how do they relate to the resistance to atrial natriuretic peptides? , 1995, Journal of cardiac failure.

[15]  S. Berti,et al.  Altered tissue degradation and distribution of atrial natriuretic peptide in patients with idiopathic dilated cardiomyopathy and its relationship with clinical severity of the disease and sodium handling. , 1995, Circulation.

[16]  R. Moreau,et al.  Blunted natriuresis and abnormal systemic hemodynamic responses to C-type and brain natriuretic peptides in rats with cirrhosis. , 1995, Journal of hepatology.

[17]  J. Leahy,et al.  Increased secretory demand rather than a defect in the proinsulin conversion mechanism causes hyperproinsulinemia in a glucose-infusion rat model of non-insulin-dependent diabetes mellitus. , 1995, The Journal of clinical investigation.

[18]  M. Packer The neurohormonal hypothesis: a theory to explain the mechanism of disease progression in heart failure. , 1992, Journal of the American College of Cardiology.

[19]  J. Rehfeld,et al.  Progastrin processing during antral G-cell hypersecretion in humans. , 1989, Gastroenterology.

[20]  C. Johnston,et al.  Decreased Atrial Natriuretic Peptide Binding in Renal Medulla in Rats With Chronic Heart Failure , 1988, Circulation research.

[21]  H. Imura,et al.  Clinical application of atrial natriuretic polypeptide in patients with congestive heart failure: beneficial effects on left ventricular function. , 1987, Circulation.

[22]  Andrew,et al.  Atrial natriuretic factor in normal subjects and heart failure patients. Plasma levels and renal, hormonal, and hemodynamic responses to peptide infusion. , 1986, The Journal of clinical investigation.

[23]  J. Rehfeld,et al.  The posttranslational phase of gene expression: new possibilities in molecular diagnosis. , 2003, Current molecular medicine.

[24]  P. Smits,et al.  Possibility of downregulation of atrial natriuretic peptide receptor coupled to guanylate cyclase in peripheral vascular beds of patients with chronic severe heart failure. , 1993, Circulation.