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Letters to the Editor |
Consiglio Nazionale delle Ricerche, Institute of Clinical Physiology, Pisa, Italy
aAddress correspondence to this author at: Laboratory of Cardiovascular Endocrinology and Cell Biology, CNR Institute of Clinical Physiology, Via Trieste 41, 56126 Pisa, Italy. Fax 39-0585-493601; e-mail clerico@ifc.cnr.it.
| The first 20% of the full text of this article appears below. |
To the Editor:
The cardiac natriuretic hormones (CNHs), atrial (ANP) and B-type natriuretic peptide (BNP), are peptides produced and secreted by the atrial and ventricular cardiomyocytes, respectively. ANP and BNP share potent diuretic, natriuretic, and vascular smooth-muscle-relaxing effects and interact with the hormonal and nervous systems (1)(2)(3). Stimulation by hemodynamic overload, as well as by several neuroendocrine (including
-adrenergic agonists, angiotensin II, endothelins, and vasopressin) and immunologic agents and by growth factors, modulates the production of CNHs by the human heart (1)(2). CNHs and their respective counter-regulatory neurohormonal systems (including the adrenergic, endothelin, and renin-angiotensin-aldosterone systems) form a physiologic negative feedback mechanism that regulates cardiac output by controlling blood pressure and heart rate as well as by fluid and electrolyte homeostasis (1)(2).
The clinical relevance of measurement of BNP and its related peptides as diagnostic tools and prognostic markers in patients with cardiovascular diseases has been confirmed recently (2)(3). To achieve correct interpretation of serial test results that are collected for follow-up or for tailored treatment
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