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Brain natriuretic peptide: Much more than a biomarker

Research output: Contribution to journalArticle

Luigino Calzetta, Augusto Orlandi, Clive Page, Paola Rogliani, Barbara Rinaldi, Giuseppe Rosano, Mario Cazzola, Maria Gabriella Matera

Original languageEnglish
JournalInternational Journal of Cardiology
DOIs
Accepted/In press7 Jul 2016

Documents

  • Brain natriuretic peptide_CALZETTA_Accepted 7Jul2016_GREEN AAM

    Brain_natriuretic_peptide_CALZETTA_Accepted_7Jul2016_GREEN_AAM.pdf, 538 KB, application/pdf

    Uploaded date:11 Jul 2016

    Version:Accepted author manuscript

    Licence:CC BY-NC-ND

    © 2016. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/

King's Authors

Abstract

Brain natriuretic peptide (BNP) modulates several biological processes by activating the natriuretic peptide receptor A (NPR-A). Atria and ventricles secrete BNP. BNP increases natriuresis, diuresis and vasodilatation, thus resulting in a decreased cardiac workload. BNP and NT-proBNP, which is the biologically inactive N-terminal portion of its pro-hormone, are fast and sensitive biomarkers for diagnosing heart failure. The plasma concentrations of both BNP and NT-proBNP also correlate with left ventricular function in patients with acute exacerbation of COPD, even without history of heart failure. Several studies have been conducted in vitro and in vivo, both in animals and in humans, in order to assess the potential role of the NPR-A activation as a novel therapeutic approach for treating obstructive pulmonary disorders. Unfortunately, these studies have yielded conflicting results. Nevertheless, further recent specific studies, performed in ex vivo models of asthma and COPD, have confirmed the bronchorelaxant effect of BNP and its protective role against bronchial hyperresponsiveness in human airways. These studies have also clarified the intimate mechanism of action of BNP, represented by an autocrine loop elicited by the activation of NPR-A, localized on bronchial epithelium, and the relaxant response of the surrounding ASM, that does not expresses NPR-A. Therefore, this review explores the teleological activities and paradoxical effects of BNP with regard of chronic obstructive respiratory disorders, and provides an excursus on the main scientific findings that explain why BNP should be considered much more than a biomarker.

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