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B-type natriuretic peptide: a treatment, not a diagnostic marker

Correspondence to:
Dr G W Yip, Division of Cardiology, S H Ho Cardiovascular and Stroke Centre, Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT Hong Kong, The People’s Republic of China; gabrielyip@cuhk.edu.hk

The first 150 words of the full text of this article appear below.

Since the discovery of atrial natriuretic peptide by de Bold and colleagues in 1981, research into the natriuretic peptide (NP) system has expanded enormously over the past 25 years.¹ It has moved beyond the role of an endocrine system that modulates volume and pressure homoeostasis in response to increased myocardial wall stress by its effects on the cardiac and renal function, through natriuresis, diuresis, vasodilatation and positive lusitropism. Increasing evidence has now established that the natriuretic peptides possess anti-fibrotic, anti-hypertrophic, anti-inflammatory, cytoprotective properties on the myocardium, in addition to suppression of the renin–angiotensin–aldosterone system, sympathetic outflow, arginine vasopressin and endothelin.²

The NP family is growing and currently consists of atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), which are produced predominantly from atria and ventricles, respectively, and also from cardiac fibroblasts; C-type natriuretic peptide (CNP) from the vascular endothelium and central nervous system; dendroaspis natriuretic peptide (DNP) synthesised based on . . . [Full text of this article]

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B-type natriuretic peptide infusions in acute myocardial infarction

R J Hillock, C M Frampton, T G Yandle, R W Troughton, J G Lainchbury, and A M Richards
Heart 2008 94: 617-622. [Abstract] [Full Text] [PDF]