Natriuretic peptides, respiratory disease, and the right heart.

It is well-recognized that atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are raised in conditions with ventricular volume and pressure overload. In addition to this established role in left ventricular congestive cardiac failure, there is good evidence that BNP has a diagnost...

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Main Authors: Yap, L, Mukerjee, D, Timms, P, Ashrafian, H, Coghlan, J
Format: Journal article
Language:English
Published: 2004
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author Yap, L
Mukerjee, D
Timms, P
Ashrafian, H
Coghlan, J
author_facet Yap, L
Mukerjee, D
Timms, P
Ashrafian, H
Coghlan, J
author_sort Yap, L
collection OXFORD
description It is well-recognized that atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are raised in conditions with ventricular volume and pressure overload. In addition to this established role in left ventricular congestive cardiac failure, there is good evidence that BNP has a diagnostic role in right ventricular (RV) dysfunction and pulmonary arterial hypertension (PAH). For example, BNP levels can be used to differentiate between dyspneic patients with pure respiratory defects and those with RV dysfunction. Studies in patients with PAH have demonstrated significant correlations between BNP levels and mean pulmonary arterial pressure as well as pulmonary vascular resistance. Additionally, BNP has a prognostic role in patients with RV pressure overload and pulmonary hypertension, and it offers a noninvasive test that can be used to guide therapy in patients with PAH. However, although measured plasma proBNP levels are raised in conditions with RV overload, its biological significance is still not well-understood. In this article, we review the general physiologic and potential therapeutic role of natriuretic peptides in respiratory disease, RV dysfunction, and PAH. Furthermore, we assess the various clues toward natriuretic peptide action coming from laboratory studies. ANP and BNP knockout mice develop cardiac fibrosis and hypertrophy. Potentiation of the natriuretic pathway has been shown to reduce cardiac hypertrophy and PAH. This is likely to take place as a result of increased intracellular cyclic guanosine monophosphate levels and subsequent pulmonary vasorelaxant activity. In view of this evidence, there may be a rationale for the therapeutic use of recombinant BNP or neutral endopeptidase inhibitors under conditions of RV dysfunction and PAH.
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spelling oxford-uuid:8d060aeb-b132-49c9-a516-59e89bce9ffa2022-03-26T22:48:27ZNatriuretic peptides, respiratory disease, and the right heart.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:8d060aeb-b132-49c9-a516-59e89bce9ffaEnglishSymplectic Elements at Oxford2004Yap, LMukerjee, DTimms, PAshrafian, HCoghlan, JIt is well-recognized that atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are raised in conditions with ventricular volume and pressure overload. In addition to this established role in left ventricular congestive cardiac failure, there is good evidence that BNP has a diagnostic role in right ventricular (RV) dysfunction and pulmonary arterial hypertension (PAH). For example, BNP levels can be used to differentiate between dyspneic patients with pure respiratory defects and those with RV dysfunction. Studies in patients with PAH have demonstrated significant correlations between BNP levels and mean pulmonary arterial pressure as well as pulmonary vascular resistance. Additionally, BNP has a prognostic role in patients with RV pressure overload and pulmonary hypertension, and it offers a noninvasive test that can be used to guide therapy in patients with PAH. However, although measured plasma proBNP levels are raised in conditions with RV overload, its biological significance is still not well-understood. In this article, we review the general physiologic and potential therapeutic role of natriuretic peptides in respiratory disease, RV dysfunction, and PAH. Furthermore, we assess the various clues toward natriuretic peptide action coming from laboratory studies. ANP and BNP knockout mice develop cardiac fibrosis and hypertrophy. Potentiation of the natriuretic pathway has been shown to reduce cardiac hypertrophy and PAH. This is likely to take place as a result of increased intracellular cyclic guanosine monophosphate levels and subsequent pulmonary vasorelaxant activity. In view of this evidence, there may be a rationale for the therapeutic use of recombinant BNP or neutral endopeptidase inhibitors under conditions of RV dysfunction and PAH.
spellingShingle Yap, L
Mukerjee, D
Timms, P
Ashrafian, H
Coghlan, J
Natriuretic peptides, respiratory disease, and the right heart.
title Natriuretic peptides, respiratory disease, and the right heart.
title_full Natriuretic peptides, respiratory disease, and the right heart.
title_fullStr Natriuretic peptides, respiratory disease, and the right heart.
title_full_unstemmed Natriuretic peptides, respiratory disease, and the right heart.
title_short Natriuretic peptides, respiratory disease, and the right heart.
title_sort natriuretic peptides respiratory disease and the right heart
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AT mukerjeed natriureticpeptidesrespiratorydiseaseandtherightheart
AT timmsp natriureticpeptidesrespiratorydiseaseandtherightheart
AT ashrafianh natriureticpeptidesrespiratorydiseaseandtherightheart
AT coghlanj natriureticpeptidesrespiratorydiseaseandtherightheart